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PSYORG.com
A team of scientists from the University of Copenhagen and the Max Planck Institute in Germany, has identified no less than 3,600 molecular switches in the human body. These switches, which regulate protein functions, may prove to be a crucial factor in human aging and the onset and treatment of diseases such as cancer, Alzheimer's disease and Parkinson's disease. The results of the team's work have been published in the current edition of the journal Science.
The team, led by Professor Matthias Mann of Novo Nordisk Center for Protein Research at the University of Copenhagen and the Max Planck Institute for Biochemistry in Germany, have detected 3,600 acetylation switches in 1,750 different proteins.
"This is more than just a technological achievement, it has also expanded the number of known acetylation switches by a factor of six, and it gives us for the first time a comprehensive insight into this type of protein modification," says Professor Mann.
A given protein can perform more than one task, and how it behaves is regulated by adding a small molecule that acts as a 'switch' which can turn on the different tasks. Acetylation is essential for cells' ability to function normally. Defective protein regulation plays a role in ageing and the development of diseases such as cancer, Parkinson's and Alzheimer's.
"With the new mapping, we can now begin to study and describe how acetylation switches respond to medications that could repair the defects on them. It can have a major impact on medical care," says Professor Mann, adding that medications to repair the damaged protein regulation are already showing promising in the treatment of cancer.
Cooperating proteins
The team also discovered that.......read all about Scientists locate disease switches
Thursday, July 30, 2009
Wednesday, July 29, 2009
Large Epidemiologic Study Supports Brain Power Of Fish In Older People
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ScienceDaily — Experts estimate that over 24 million people worldwide suffer from dementia, and many of these people live in low- and middle-income countries. Recently, there has been growing interest in whether dietary factors, particularly oily fish and meat, might influence the onset and/or severity of dementia. Oily fish are rich in omega-3 long-chain polyunsaturated fatty acids, which some studies suggest are positively related to cognitive function in later life.
Conversely, there is a suggestion from some studies that increased meat consumption may be related to cognitive decline. To examine this, a group of international researchers studied older people in 7 middle- to low-income countries. You can read the results of their study in the August 2009 issue of the American Journal of Clinical Nutrition.
Data from 14,960 participants (≥65 y of age) living in China, India, Cuba, the Dominican Republic, Venezuela, Mexico, and Peru were analyzed. Dietary habits were assessed by using standard, culturally appropriate face-to-face interviews, and dementia was diagnosed by using validated culturally and educationally fair criteria.
In each of the study countries, except India, there was an inverse association between fish consumption and dementia prevalence. These data extend to low- and middle-income countries previous conclusions from industrialized countries that increased fish consumption is associated with lower dementia prevalence in later life.
The authors propose that this....read more of how a Large Epidemiologic Study Supports Brain Power Of Fish In Older People
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ScienceDaily — Experts estimate that over 24 million people worldwide suffer from dementia, and many of these people live in low- and middle-income countries. Recently, there has been growing interest in whether dietary factors, particularly oily fish and meat, might influence the onset and/or severity of dementia. Oily fish are rich in omega-3 long-chain polyunsaturated fatty acids, which some studies suggest are positively related to cognitive function in later life.
Conversely, there is a suggestion from some studies that increased meat consumption may be related to cognitive decline. To examine this, a group of international researchers studied older people in 7 middle- to low-income countries. You can read the results of their study in the August 2009 issue of the American Journal of Clinical Nutrition.
Data from 14,960 participants (≥65 y of age) living in China, India, Cuba, the Dominican Republic, Venezuela, Mexico, and Peru were analyzed. Dietary habits were assessed by using standard, culturally appropriate face-to-face interviews, and dementia was diagnosed by using validated culturally and educationally fair criteria.
In each of the study countries, except India, there was an inverse association between fish consumption and dementia prevalence. These data extend to low- and middle-income countries previous conclusions from industrialized countries that increased fish consumption is associated with lower dementia prevalence in later life.
The authors propose that this....read more of how a Large Epidemiologic Study Supports Brain Power Of Fish In Older People
Monday, July 27, 2009
Hunt for Alzheimer's disease treatment intensifies
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Chicago Tribune
Drugmakers, including Abbott and Baxter, increase efforts despite setbacks
By Bruce Japsen | Tribune reporter
Just two weeks ago, word came from an international science meeting in Vienna that Abbott Laboratories had halted a study of an Alzheimer's pill, the latest in a growing number of pharmaceutical company failures related to treatment of the disease.
But the North Chicago-based medical products company and its rivals are hardly giving up.
"This is an area where the reward is so great and the unmet need is so high we are going to continue to be involved," said James Summers, head of Abbott's neuroscience drug discovery.
The payoff for treatments would be worth billions of dollars, especially as the world's population ages. The disease and related dementia affect more than 5 million Americans and 30 million people around the world. But the worldwide number is expected to rise fourfold, to 120 million people by 2050.
Abbott is competing against Deerfield-based Baxter International Inc., as well as drugmakers such as Pfizer Inc., Johnson & Johnson and Wyeth, that say they are making unprecedented investments in what has been an elusive treatment category.
"What is a positive about the increasing investments is that.......read more of
Alzheimer's disease treatment intensifies
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Chicago Tribune
Drugmakers, including Abbott and Baxter, increase efforts despite setbacks
By Bruce Japsen | Tribune reporter
Just two weeks ago, word came from an international science meeting in Vienna that Abbott Laboratories had halted a study of an Alzheimer's pill, the latest in a growing number of pharmaceutical company failures related to treatment of the disease.
But the North Chicago-based medical products company and its rivals are hardly giving up.
"This is an area where the reward is so great and the unmet need is so high we are going to continue to be involved," said James Summers, head of Abbott's neuroscience drug discovery.
The payoff for treatments would be worth billions of dollars, especially as the world's population ages. The disease and related dementia affect more than 5 million Americans and 30 million people around the world. But the worldwide number is expected to rise fourfold, to 120 million people by 2050.
Abbott is competing against Deerfield-based Baxter International Inc., as well as drugmakers such as Pfizer Inc., Johnson & Johnson and Wyeth, that say they are making unprecedented investments in what has been an elusive treatment category.
"What is a positive about the increasing investments is that.......read more of
Alzheimer's disease treatment intensifies
Sunday, July 26, 2009
Pesticides May Raise Alzheimer's Risk
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WebMD
Alzheimer's Disease Health Center
Occupational Exposure Linked to Increased Risk of Alzheimer's Disease
By Charlene Laino
WebMD Health News
Reviewed by Louise Chang, MD
(Vienna, Austria) -- Exposure to pesticides may have long-term effects on the nervous system, increasing the risk of Alzheimer’s disease in late life, a new study suggests.
Researchers say the findings support evidence of a possible link between environmental toxins and Alzheimer’s disease and may help explain why some people with risk factors for the disease get it while others do not.
“While no cause for Alzheimer’s disease has been found, [non-inherited] cases are likely due to a combination of genetic and environmental factors,” says Kathleen M. Hayden, PhD, of Duke University Medical Center in Durham, N.C.
Pesticides and Alzheimer’s
Pesticides have been proposed as a possible environmental risk factor, but there are few studies of the effects of occupational pesticides on the risk of Alzheimer’s disease, she says.
Research suggests that pesticides may affect the release of acetylcholine, a chemical that’s important for memory, Hayden tells WebMD.
Pesticide use has dramatically increased over the past 50 years, she says. There are now more than 18,000 pesticides licensed in the U.S., and more than 2 billion pounds are applied each year, Hayden says.
There are 5.3 million Americans living with Alzheimer’s disease, which disrupts memory, learning, and other mental functions. By 2010, there will be nearly half a million new cases each year and by 2050, there will be nearly a million new cases annually, according to the Alzheimer’s Association.
Working With Pesticides
The new study involved more than 4,000 residents 65 and older from an agricultural county in Utah who are participating in a larger study of risk factors for Alzheimer’s disease.
At the start of study, they were asked if they had ever been exposed to pesticides during their work and if so, which types of pesticide and for how long. Of the total, about 750 participants reported working with pesticides.
A standard test that measures overall cognitive function, including memory, attention span, and problem solving, was given at the outset and two other times over a six- to seven-year period.
The study was presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease.
Pesticides Linked to Alzheimer’s
After adjusting for age, sex, education, and a gene known to raise the risk of Alzheimer’s, the researchers found that people who worked with pesticides were 53% more likely to develop Alzheimer’s disease.
The study doesn’t prove that pesticides cause Alzheimer’s disease, and further research is needed, Hayden says.
The next steps are to look at whether type of pesticide and duration of use affects risk, she says.
Ralph Nixon, MD, PhD, vice chair of the Medical and Scientific Advisory Council at the Alzheimer’s Association and an Alzheimer’s expert at New York University, tells WebMD that it’s been difficult to identifyread more about Pesticides Linked to Alzheimer’s
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WebMD
Alzheimer's Disease Health Center
Occupational Exposure Linked to Increased Risk of Alzheimer's Disease
By Charlene Laino
WebMD Health News
Reviewed by Louise Chang, MD
(Vienna, Austria) -- Exposure to pesticides may have long-term effects on the nervous system, increasing the risk of Alzheimer’s disease in late life, a new study suggests.
Researchers say the findings support evidence of a possible link between environmental toxins and Alzheimer’s disease and may help explain why some people with risk factors for the disease get it while others do not.
“While no cause for Alzheimer’s disease has been found, [non-inherited] cases are likely due to a combination of genetic and environmental factors,” says Kathleen M. Hayden, PhD, of Duke University Medical Center in Durham, N.C.
Pesticides and Alzheimer’s
Pesticides have been proposed as a possible environmental risk factor, but there are few studies of the effects of occupational pesticides on the risk of Alzheimer’s disease, she says.
Research suggests that pesticides may affect the release of acetylcholine, a chemical that’s important for memory, Hayden tells WebMD.
Pesticide use has dramatically increased over the past 50 years, she says. There are now more than 18,000 pesticides licensed in the U.S., and more than 2 billion pounds are applied each year, Hayden says.
There are 5.3 million Americans living with Alzheimer’s disease, which disrupts memory, learning, and other mental functions. By 2010, there will be nearly half a million new cases each year and by 2050, there will be nearly a million new cases annually, according to the Alzheimer’s Association.
Working With Pesticides
The new study involved more than 4,000 residents 65 and older from an agricultural county in Utah who are participating in a larger study of risk factors for Alzheimer’s disease.
At the start of study, they were asked if they had ever been exposed to pesticides during their work and if so, which types of pesticide and for how long. Of the total, about 750 participants reported working with pesticides.
A standard test that measures overall cognitive function, including memory, attention span, and problem solving, was given at the outset and two other times over a six- to seven-year period.
The study was presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease.
Pesticides Linked to Alzheimer’s
After adjusting for age, sex, education, and a gene known to raise the risk of Alzheimer’s, the researchers found that people who worked with pesticides were 53% more likely to develop Alzheimer’s disease.
The study doesn’t prove that pesticides cause Alzheimer’s disease, and further research is needed, Hayden says.
The next steps are to look at whether type of pesticide and duration of use affects risk, she says.
Ralph Nixon, MD, PhD, vice chair of the Medical and Scientific Advisory Council at the Alzheimer’s Association and an Alzheimer’s expert at New York University, tells WebMD that it’s been difficult to identifyread more about Pesticides Linked to Alzheimer’s
Friday, July 24, 2009
Symptoms Of Alzheimer's May Come In Your 50s
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abcnews.com
Gene Study Shows Earlier Signs of Memory Loss, Hints at Earlier Intervention
By JOSEPH BROWNSTEIN
ABC News Medical Unit
For people with a common genetic variation, researchers have discovered signs of the possible onset of Alzheimer's before a patient would be clinically diagnosed by a doctor.
In people with the ApoE4 gene variation, one previously implicated as affecting the likelihood of Alzheimer's, researchers have been able to pinpoint some signs of memory loss beginning in the person's mid- to late-50s -- without the patient having full-blown Alzheimer's disease or dementia.
"[One could argue] we really captured for the first time the onset of Alzheimer's disease," explained Dr. Richard Caselli, a neurologist at the Mayo Clinic in Scottsdale, Ariz.
"What's passing as normal aging itself correlates with the most common genetic risk factor for Alzheimer's disease," he said, adding that the symptoms are noticeable in a clinical setting, but not in everyday life.
"It's not the sort of thing that you can look at somebody or they can look at themselves and know."
Researchers caution that when......read all of Health Alzheimer's News Story
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abcnews.com
Gene Study Shows Earlier Signs of Memory Loss, Hints at Earlier Intervention
By JOSEPH BROWNSTEIN
ABC News Medical Unit
For people with a common genetic variation, researchers have discovered signs of the possible onset of Alzheimer's before a patient would be clinically diagnosed by a doctor.
In people with the ApoE4 gene variation, one previously implicated as affecting the likelihood of Alzheimer's, researchers have been able to pinpoint some signs of memory loss beginning in the person's mid- to late-50s -- without the patient having full-blown Alzheimer's disease or dementia.
"[One could argue] we really captured for the first time the onset of Alzheimer's disease," explained Dr. Richard Caselli, a neurologist at the Mayo Clinic in Scottsdale, Ariz.
"What's passing as normal aging itself correlates with the most common genetic risk factor for Alzheimer's disease," he said, adding that the symptoms are noticeable in a clinical setting, but not in everyday life.
"It's not the sort of thing that you can look at somebody or they can look at themselves and know."
Researchers caution that when......read all of Health Alzheimer's News Story
Thursday, July 23, 2009
A puzzling finding for promising Alzheimer's drug
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LA Times
Many researchers believe that one way to treat symptoms of Alzheimer's disease is with drugs that reduce a substance called beta amyloid. This is a protein that is the main constituent of plaques found in the brains of people with the disease.
But in a surprising finding presented Wednesday at the Alzheimer's Assn. 2009 International Conference in Vienna, researchers discovered that a promising medication in phase-3 testing in the United States, called dimebolin or Dimebon, actually increases beta amyloid in the brain in animal models.
"This result is highly unexpected in what may prove to be a clinically beneficial Alzheimer's drug," Dr. Samuel Gandy, the lead author of the study, said in a news release. "We need more research to further clarify how dimebolin affects beta amyloid levels in the brain."
Previous studies show that Dimebon, which was used for years in Russia as an antihistamine, appears to help people suffering from mild to moderate Alzheimer's disease symptoms. In June, enrollment was completed for a six-month pivotal trial of the medication. The manufacturer, Medivation Inc., has announced it hopes to file a new drug application for Dimebon in 2011.
Researchers can't explain why Dimebon appears to be helpful even though it increases beta amyloid. It could be the drug's beneficial powers have nothing to do with amyloid. This theory would point to a new avenue of drug targets for treating Alzheimer's disease.
In other news from the Alzheimer's meeting:
A large study of people with mild cognitive impairment showed that the combination of cognitive tests and brain scans can be used to predict the development of Alzheimer's disease.
Researchers at UC Berkeley studied 85 people with mild cognitive impairment. Those with low scores on a memory recall test and low glucose metabolism in a particular brain region (measured by PET scan) had a 15-times greater risk of developing Alzheimer's disease within two years of the study compared with the other participants.
"By the time a patient is diagnosed with Alzheimer's disease, there is usually little one can do to stop or reverse the decline," Dr. William Jagust, the principal investigator of the study, said in a news release. "Researchers are trying to determine whether treating patients before severe symptoms appear will be more effective, and that requires better diagnostic tools than what is currently available."
Several studies have found that middle-age people who have moderate alcohol intake, such as a glass of wine a day, receive some long-term protection against cognitive decline and dementia in old age. A new study, the largest and longest to examine regular alcohol intake on dementia in seniors, has found that this protection also applies in old age. But there is one important exception: People who already have mild cognitive impairment might fare worse if they drink alcohol.
The study examined 3,069 people ages 75 and older about their drinking habits. The participants were examined and interviewed every six months for six years. The study showed that in people with no cognitive impairment at the start of the study, drinking eight to 14 alcoholic beverages a week resulted in a 27% reduction in the risk of developing dementia compared with people who did not drink at all. But for older adults with mild cognitive impairment, any consumption of alcohol was linked to
------read all about promising Alzheimer's drug
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LA Times
Many researchers believe that one way to treat symptoms of Alzheimer's disease is with drugs that reduce a substance called beta amyloid. This is a protein that is the main constituent of plaques found in the brains of people with the disease.
But in a surprising finding presented Wednesday at the Alzheimer's Assn. 2009 International Conference in Vienna, researchers discovered that a promising medication in phase-3 testing in the United States, called dimebolin or Dimebon, actually increases beta amyloid in the brain in animal models.
"This result is highly unexpected in what may prove to be a clinically beneficial Alzheimer's drug," Dr. Samuel Gandy, the lead author of the study, said in a news release. "We need more research to further clarify how dimebolin affects beta amyloid levels in the brain."
Previous studies show that Dimebon, which was used for years in Russia as an antihistamine, appears to help people suffering from mild to moderate Alzheimer's disease symptoms. In June, enrollment was completed for a six-month pivotal trial of the medication. The manufacturer, Medivation Inc., has announced it hopes to file a new drug application for Dimebon in 2011.
Researchers can't explain why Dimebon appears to be helpful even though it increases beta amyloid. It could be the drug's beneficial powers have nothing to do with amyloid. This theory would point to a new avenue of drug targets for treating Alzheimer's disease.
In other news from the Alzheimer's meeting:
A large study of people with mild cognitive impairment showed that the combination of cognitive tests and brain scans can be used to predict the development of Alzheimer's disease.
Researchers at UC Berkeley studied 85 people with mild cognitive impairment. Those with low scores on a memory recall test and low glucose metabolism in a particular brain region (measured by PET scan) had a 15-times greater risk of developing Alzheimer's disease within two years of the study compared with the other participants.
"By the time a patient is diagnosed with Alzheimer's disease, there is usually little one can do to stop or reverse the decline," Dr. William Jagust, the principal investigator of the study, said in a news release. "Researchers are trying to determine whether treating patients before severe symptoms appear will be more effective, and that requires better diagnostic tools than what is currently available."
Several studies have found that middle-age people who have moderate alcohol intake, such as a glass of wine a day, receive some long-term protection against cognitive decline and dementia in old age. A new study, the largest and longest to examine regular alcohol intake on dementia in seniors, has found that this protection also applies in old age. But there is one important exception: People who already have mild cognitive impairment might fare worse if they drink alcohol.
The study examined 3,069 people ages 75 and older about their drinking habits. The participants were examined and interviewed every six months for six years. The study showed that in people with no cognitive impairment at the start of the study, drinking eight to 14 alcoholic beverages a week resulted in a 27% reduction in the risk of developing dementia compared with people who did not drink at all. But for older adults with mild cognitive impairment, any consumption of alcohol was linked to
------read all about promising Alzheimer's drug
Wednesday, July 22, 2009
Want to Live Forever? Antibiotic May Prevent Age-Related Disease in People
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Attorneyatlaw.com
Ever since Spanish explorer Juan Ponce de Leon set out for the New World to find the mythological Fountain of Youth, man has yearned to unlock the mysteries to staying forever young.
Now, 500 years after de Leon’s failed mission (he died in July 1521), medical researchers say an antibiotic pill designed to prevent organ transplant rejection has been shown to help laboratory mice live longer.
The drug, marketed under the brand name Rapamune but known generically as rapamycin or siroliumus, may also someday serve another purpose: Helping extend the lives of people battling age-related disease such as Alzheimer’s disease, cancer, heart disease, and other disorders, researchers said.
“Rapamycin may extend lifespan by postponing death from cancer, by retarding mechanisms of aging, or both,” David Harrison of The Jackson Laboratory in Bar Harbor, Maine and colleagues wrote in their report, published in the journal Nature, according to a Reuters news report.
Lab Rats Live Longer
In laboratory testing, adult female mice given Rapamycin lived 14 percent longer, while male mice given the drug lived nine percent longer lives, the researchers said.
However, people shouldn’t start taking Rapamycin pills daily in an effort to live longer lives, the research team cautioned. For one thing, mice in the experiment were not exposed to any infection, which could have significantly affected the study results. Also, mice do not tend to biologically age the same way as people and tend to live much shorter lives than humans.
Researchers across the United States gave.......read all about Antibiotic that prevents age related disease
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Attorneyatlaw.com
Ever since Spanish explorer Juan Ponce de Leon set out for the New World to find the mythological Fountain of Youth, man has yearned to unlock the mysteries to staying forever young.
Now, 500 years after de Leon’s failed mission (he died in July 1521), medical researchers say an antibiotic pill designed to prevent organ transplant rejection has been shown to help laboratory mice live longer.
The drug, marketed under the brand name Rapamune but known generically as rapamycin or siroliumus, may also someday serve another purpose: Helping extend the lives of people battling age-related disease such as Alzheimer’s disease, cancer, heart disease, and other disorders, researchers said.
“Rapamycin may extend lifespan by postponing death from cancer, by retarding mechanisms of aging, or both,” David Harrison of The Jackson Laboratory in Bar Harbor, Maine and colleagues wrote in their report, published in the journal Nature, according to a Reuters news report.
Lab Rats Live Longer
In laboratory testing, adult female mice given Rapamycin lived 14 percent longer, while male mice given the drug lived nine percent longer lives, the researchers said.
However, people shouldn’t start taking Rapamycin pills daily in an effort to live longer lives, the research team cautioned. For one thing, mice in the experiment were not exposed to any infection, which could have significantly affected the study results. Also, mice do not tend to biologically age the same way as people and tend to live much shorter lives than humans.
Researchers across the United States gave.......read all about Antibiotic that prevents age related disease
Monday, July 20, 2009
Hypertrophy May Be the Key to Silent Alzheimer's Disease
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Modern Medicine
Neuronal hypertrophy more common in those with asymptomatic form of disease
(HealthDay News) -- The brain cells of people with asymptomatic Alzheimer's disease undergo significant hypertrophy, which may be a compensatory mechanism to prevent cognitive impairment, according to a study published online July 8 in Neurology.
Diego Iacono, M.D., of Johns Hopkins University in Baltimore, Md., and colleagues measured the volumes of neuronal cell bodies, nuclei and nucleoli in the CA1 region of the hippocampus of four groups of subjects: 10 with asymptomatic Alzheimer's disease, five with mild cognitive impairment, 10 with Alzheimer's disease, and 13 age-matched controls. They also compared the linguistic ability of all groups in early life.
Among the subjects with asymptomatic Alzheimer's disease, there were significantly greater degrees of hypertrophy compared to the subjects with mild cognitive impairment, at 44.9 percent more for cell bodies, 59.7 percent for nuclei, and 80.2 percent for nucleoli, the investigators found. Subjects in the control and asymptomatic Alzheimer's disease groups also had significantly higher idea density scores than their counterparts in the mild cognitive impairment and Alzheimer's disease groups.
"The major finding of the present study is the significant read all about Hypertrophy and Alzheimer's disease
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Modern Medicine
Neuronal hypertrophy more common in those with asymptomatic form of disease
(HealthDay News) -- The brain cells of people with asymptomatic Alzheimer's disease undergo significant hypertrophy, which may be a compensatory mechanism to prevent cognitive impairment, according to a study published online July 8 in Neurology.
Diego Iacono, M.D., of Johns Hopkins University in Baltimore, Md., and colleagues measured the volumes of neuronal cell bodies, nuclei and nucleoli in the CA1 region of the hippocampus of four groups of subjects: 10 with asymptomatic Alzheimer's disease, five with mild cognitive impairment, 10 with Alzheimer's disease, and 13 age-matched controls. They also compared the linguistic ability of all groups in early life.
Among the subjects with asymptomatic Alzheimer's disease, there were significantly greater degrees of hypertrophy compared to the subjects with mild cognitive impairment, at 44.9 percent more for cell bodies, 59.7 percent for nuclei, and 80.2 percent for nucleoli, the investigators found. Subjects in the control and asymptomatic Alzheimer's disease groups also had significantly higher idea density scores than their counterparts in the mild cognitive impairment and Alzheimer's disease groups.
"The major finding of the present study is the significant read all about Hypertrophy and Alzheimer's disease
Sunday, July 19, 2009
MicroRNAs Hold Promise For Treating Diseases In Blood Vessels
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ScienceDaily-- A newly discovered mechanism controls whether muscle cells in blood vessels hasten the development of both atherosclerosis and Alzheimer's disease, according to an article published online July 5 in the journal Nature.
The study was led by the Gladstone Institute of Cardiovascular Disease (GICD) in San Francisco, with key contributions from the Aab Cardiovascular Research Institute at the University of Rochester School of Medicine and Dentistry.
Thanks to stem cells, humans develop from a single cell embryo into a complex being with about 250 unique cell types. As the fetus develops, cells divide and multiply (proliferate) in many generations and specialize (differentiate) with each generation until millions of functional cells result (bone, nerve, blood, skin, muscle, etc.). To serve specific roles in the body, some stem cells also switch back and forth between primitive, rapidly proliferating precursors and their mature, functioning, non-proliferating counterparts, a quality called "plasticity."
Among the most "plastic" of cells are vascular smooth muscle cells (VSMC), which form in layers around blood vessels, and by contracting or relaxing, regulate blood pressure. Because VSMC surround blood vessels that are continually becoming clogged by atherosclerosis, they must be ever ready to grow along with the vessel as it attempts, by growing, to remain open to blood flow despite fatty deposits and inflammation. If these efforts fail, heart attack or stoke may occur. Each time a vessel grows to avoid a clog, the VSMC surrounding it must grow too by reverting to their high-growth precursor form. Once a vessel reaches its growth limit, however, the growth that once kept vessels open begins adding to clogs by thickening vessel walls.
Past studies in Rochester have shown.........read all about MicroRNAs treating blood vessell diseases
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
ScienceDaily-- A newly discovered mechanism controls whether muscle cells in blood vessels hasten the development of both atherosclerosis and Alzheimer's disease, according to an article published online July 5 in the journal Nature.
The study was led by the Gladstone Institute of Cardiovascular Disease (GICD) in San Francisco, with key contributions from the Aab Cardiovascular Research Institute at the University of Rochester School of Medicine and Dentistry.
Thanks to stem cells, humans develop from a single cell embryo into a complex being with about 250 unique cell types. As the fetus develops, cells divide and multiply (proliferate) in many generations and specialize (differentiate) with each generation until millions of functional cells result (bone, nerve, blood, skin, muscle, etc.). To serve specific roles in the body, some stem cells also switch back and forth between primitive, rapidly proliferating precursors and their mature, functioning, non-proliferating counterparts, a quality called "plasticity."
Among the most "plastic" of cells are vascular smooth muscle cells (VSMC), which form in layers around blood vessels, and by contracting or relaxing, regulate blood pressure. Because VSMC surround blood vessels that are continually becoming clogged by atherosclerosis, they must be ever ready to grow along with the vessel as it attempts, by growing, to remain open to blood flow despite fatty deposits and inflammation. If these efforts fail, heart attack or stoke may occur. Each time a vessel grows to avoid a clog, the VSMC surrounding it must grow too by reverting to their high-growth precursor form. Once a vessel reaches its growth limit, however, the growth that once kept vessels open begins adding to clogs by thickening vessel walls.
Past studies in Rochester have shown.........read all about MicroRNAs treating blood vessell diseases
Saturday, July 18, 2009
Middle-Aged Widows Have Highest Dementia Risk, Research Shows
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Bloomberg.com
By Chantal Britt
Bloomberg) -- People over 50 who suffer from negative emotions and disruption when they lose their partners have the highest risk of developing Alzheimer’s disease, according to a study published in the British Medical Journal.
Being widowed or divorced in mid-life carries three times the risk, while singles have double the risk of getting dementia than people who are married or cohabiting, according to a study from researchers in Sweden and Finland.
“Supportive intervention for individuals who have lost a partner might be a promising strategy in preventive health care,” lead researcher Krister Hakansson from Vaxjo University and the Karolinska Institute in Stockholm wrote in the study.
The number of dementia sufferers is forecast to increase to more than 80 million in 2040 from about 25 million in 2005, the researchers wrote. Higher education levels, physical exercise, mentally demanding work, top jobs and leisure and intellectual activities have been shown to protect against dementia, they said.
The researchers followed 1,449 people aged 65 to 79 years living in the Kuopio and Joensuu regions in eastern Finland for an average of 21 years to see whether their marital status affected the development of dementia later in life.
The dementia and Alzheimer’s disease risk increased if people lost their partners or got divorced, Hakansson found. The highest risk occurred in people who lost their partners or got divorced and also had a known genetic risk factor that’s associated with the development of Alzheimer’s disease.
These results add to a growing body of evidence that social factors may help sustain healthy brain functioning, Hakansson said. The development of cognitive impairment and dementia is a long process that’s affected by various factors throughout life, epidemiologist Catherine Helmer said in an editorial.
Research should now focus on..........read all of Middle-Aged Widows Have Highest Dementia Risk
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Bloomberg.com
By Chantal Britt
Bloomberg) -- People over 50 who suffer from negative emotions and disruption when they lose their partners have the highest risk of developing Alzheimer’s disease, according to a study published in the British Medical Journal.
Being widowed or divorced in mid-life carries three times the risk, while singles have double the risk of getting dementia than people who are married or cohabiting, according to a study from researchers in Sweden and Finland.
“Supportive intervention for individuals who have lost a partner might be a promising strategy in preventive health care,” lead researcher Krister Hakansson from Vaxjo University and the Karolinska Institute in Stockholm wrote in the study.
The number of dementia sufferers is forecast to increase to more than 80 million in 2040 from about 25 million in 2005, the researchers wrote. Higher education levels, physical exercise, mentally demanding work, top jobs and leisure and intellectual activities have been shown to protect against dementia, they said.
The researchers followed 1,449 people aged 65 to 79 years living in the Kuopio and Joensuu regions in eastern Finland for an average of 21 years to see whether their marital status affected the development of dementia later in life.
The dementia and Alzheimer’s disease risk increased if people lost their partners or got divorced, Hakansson found. The highest risk occurred in people who lost their partners or got divorced and also had a known genetic risk factor that’s associated with the development of Alzheimer’s disease.
These results add to a growing body of evidence that social factors may help sustain healthy brain functioning, Hakansson said. The development of cognitive impairment and dementia is a long process that’s affected by various factors throughout life, epidemiologist Catherine Helmer said in an editorial.
Research should now focus on..........read all of Middle-Aged Widows Have Highest Dementia Risk
Thursday, July 16, 2009
Research reveals how Alzheimer's spreads within the brain
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Sciencecentic.com
A research in mice has demonstrated how tangles of a so-called tau protein can spread within the brain. Tangled masses of that tau protein contribute to several neurodegenerative diseases - those that destroy brain functions - including Alzheimer's disease. The research has provided insights into how tau tangles spread that allow comparisons with the way prions, those that cause Creutzfeldt-Jakob Disease, destroy brain tissue.
Dr Michel Goedert of the Medical Research Council Laboratory of Molecular Biology in Cambridge contributed to the study alongside colleagues in Switzerland and Germany and the results are published today in the online edition of Nature Cell Biology.
Speaking about the study, Dr Goedert made it clear that it would be incorrect to suggest that Alzheimer's could be contagious: 'This research in mice does not show that tau pathology is contagious or that it can spread easily from mouse to mouse. What it has revealed is how tau tangles spread within brain tissues of individual mice. It suggests that tangles of proteins that build up in the brain to cause symptoms could have some contagious properties, within brain tissue but not between mice that haven't been injected with tissue from another mouse and certainly not between people. The work describes an experimental system that will allow scientists to study the mechanisms that underlie the transmission and spread of the tangles of tau proteins connected to the symptoms of Alzheimer's disease.'
Transgenic and wild-type mice were used in the study. Transgenic mice are genetically modified to carry specific genes. In this study the mice expressed the genes for the human versions of tau proteins.
The researchers injected brain tissue from mice modified to carry the gene for the form of human tau protein implicated in neurodegenerative disease into mice that carried the normal version of the human tau protein and therefore did not already have tangles in their brain tissue. They found that the injected material went on to create tangles of tau at the injection sites. Over time, the tau tangles then spread to neighbouring regions of the brain.
In another experiment, extract from the brains of mice with the gene for mutant-human-tau was injected into the brains of a wild-type mice. In comparison to the mice transgenic for human-tau, a smaller number of tau tangles developed where the tissue was injected and there was no evidence of the tau spreading throughout the brain.
Dr Goedert concluded: 'In contrast to prion diseases, human tauopathies like Alzheimer's are believed not....read all of how Alzheimer's spreads within the brain
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Sciencecentic.com
A research in mice has demonstrated how tangles of a so-called tau protein can spread within the brain. Tangled masses of that tau protein contribute to several neurodegenerative diseases - those that destroy brain functions - including Alzheimer's disease. The research has provided insights into how tau tangles spread that allow comparisons with the way prions, those that cause Creutzfeldt-Jakob Disease, destroy brain tissue.
Dr Michel Goedert of the Medical Research Council Laboratory of Molecular Biology in Cambridge contributed to the study alongside colleagues in Switzerland and Germany and the results are published today in the online edition of Nature Cell Biology.
Speaking about the study, Dr Goedert made it clear that it would be incorrect to suggest that Alzheimer's could be contagious: 'This research in mice does not show that tau pathology is contagious or that it can spread easily from mouse to mouse. What it has revealed is how tau tangles spread within brain tissues of individual mice. It suggests that tangles of proteins that build up in the brain to cause symptoms could have some contagious properties, within brain tissue but not between mice that haven't been injected with tissue from another mouse and certainly not between people. The work describes an experimental system that will allow scientists to study the mechanisms that underlie the transmission and spread of the tangles of tau proteins connected to the symptoms of Alzheimer's disease.'
Transgenic and wild-type mice were used in the study. Transgenic mice are genetically modified to carry specific genes. In this study the mice expressed the genes for the human versions of tau proteins.
The researchers injected brain tissue from mice modified to carry the gene for the form of human tau protein implicated in neurodegenerative disease into mice that carried the normal version of the human tau protein and therefore did not already have tangles in their brain tissue. They found that the injected material went on to create tangles of tau at the injection sites. Over time, the tau tangles then spread to neighbouring regions of the brain.
In another experiment, extract from the brains of mice with the gene for mutant-human-tau was injected into the brains of a wild-type mice. In comparison to the mice transgenic for human-tau, a smaller number of tau tangles developed where the tissue was injected and there was no evidence of the tau spreading throughout the brain.
Dr Goedert concluded: 'In contrast to prion diseases, human tauopathies like Alzheimer's are believed not....read all of how Alzheimer's spreads within the brain
Wednesday, July 15, 2009
DEMENTIA: MORE THAN JUST AN AGED CARE ISSUE
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Australian Aging Agenda
Dementia is not just a concern for aged care providers but a pressing public health issue, according to the CEO of Alzheimer’s Australia.
Glenn Rees told a summit on Australia’s ageing population that dementia is a chronic condition that requires coordinated care planning.
The number of people with dementia is set to double by 2030 and without immediate government action, this could have serious effects on the health system.
Mr Rees told the forum that there should be a bigger focus on dementia in primary and acute care, noting that hospitals can be “dangerous” places for people with dementia.
“I believe there is a need to provide incentives through Medicare to promote timely and accurate diagnosis and ongoing support for people with dementia and their family carers,” he said.
“Australia should follow the lead of the UK National Healthcare Service in developing a five year strategy to train all GPs in dementia diagnosis and to support them with specialist services.”
Mr Rees praised the former government forlaunching the Dementia Initiative 2005, which led to the development of the EACH [Extended Aged Care at Home] Dementia packages.
But he reiterated the recommendations of last month’s Access Economics report, calling for more appropriate dementia respite services, revisions to the aged care planning process and quality standards for dementia ca
Turning to aged care staff interactions with people who have dementia, Mr Rees highlighted the importance of about.......aging care agenda
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Australian Aging Agenda
Dementia is not just a concern for aged care providers but a pressing public health issue, according to the CEO of Alzheimer’s Australia.
Glenn Rees told a summit on Australia’s ageing population that dementia is a chronic condition that requires coordinated care planning.
The number of people with dementia is set to double by 2030 and without immediate government action, this could have serious effects on the health system.
Mr Rees told the forum that there should be a bigger focus on dementia in primary and acute care, noting that hospitals can be “dangerous” places for people with dementia.
“I believe there is a need to provide incentives through Medicare to promote timely and accurate diagnosis and ongoing support for people with dementia and their family carers,” he said.
“Australia should follow the lead of the UK National Healthcare Service in developing a five year strategy to train all GPs in dementia diagnosis and to support them with specialist services.”
Mr Rees praised the former government forlaunching the Dementia Initiative 2005, which led to the development of the EACH [Extended Aged Care at Home] Dementia packages.
But he reiterated the recommendations of last month’s Access Economics report, calling for more appropriate dementia respite services, revisions to the aged care planning process and quality standards for dementia ca
Turning to aged care staff interactions with people who have dementia, Mr Rees highlighted the importance of about.......aging care agenda
Tuesday, July 14, 2009
Great ideas, but what's the cost?
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
PressRepublican.com
The American Association of Retired Persons, characteristically, has firm opinions on what should be included in any health-care-reform package Congress puts together. Typically, those opinions make great sense. But before this newspaper embraces AARP's suggestions, the matter of cost will have to be spelled out, which to date it hasn't.
AARP has six features it wants included in any legislation to be considered:
Extending Medicaid coverage to people between 50 and 64. Currently, a person must be 65 to qualify for coverage. This is the provision that causes most concern, since it seems to represent an enormous increase in cost.
However, Bill Ferris, legislative representative in AARP's New York State Legislative Office, explained the organization's justification in a meeting last week with the Press-Republican's Editorial Board this way: On a strictly humanitarian level, the coverage is essential so that all — or, at least, more — of the needy are taken care of. It is unacceptable that our humane, empathetic nation would leave so much of its population without access to medicine and health care. On a financial level, getting treatment for the now-uncovered needy leads to deep and expensive health problems by the time they reach their 65th birthday. Getting them treated early would relieve a lot of that cost.
He admits that the specific figures haven't been calculated yet, but that final reckoning has to figure prominently into any argument over extending Medicare coverage.
Closing a Medicaid coverage gap that now exists between annual drug costs of between $2,700 and $6,154. Below $2,700 and above $6,154, patients can receive subsidies. Between them, there is nothing. AARP wants the government close what is known as this non-coverage "doughnut hole."
Lowering drug costs through generic biologics. Biologic drugs, used against our most serious diseases, are also our most expensive. According to Ferris, the Food and Drug Administration now has no authority to grant approval for less-expensive generics.
Offering a follow-up care benefit to prevent costly hospital readmissions.
Developing a system of long-term care wherein patients are encouraged and enabled to live at home rather than in nursing homes.
Increasing availability of low-cost care, not just for the elderly but for low-income patients, as well — extending medical benefits to Medicaid recipients, of whom there are 28,000 in Clinton, Essex and Franklin counties now, according to Erin K. Mitchell, AARP associate state director.
AARP says some of the huge outlay of money could become.......read all of the Great ideas, but what's the cost
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
PressRepublican.com
The American Association of Retired Persons, characteristically, has firm opinions on what should be included in any health-care-reform package Congress puts together. Typically, those opinions make great sense. But before this newspaper embraces AARP's suggestions, the matter of cost will have to be spelled out, which to date it hasn't.
AARP has six features it wants included in any legislation to be considered:
Extending Medicaid coverage to people between 50 and 64. Currently, a person must be 65 to qualify for coverage. This is the provision that causes most concern, since it seems to represent an enormous increase in cost.
However, Bill Ferris, legislative representative in AARP's New York State Legislative Office, explained the organization's justification in a meeting last week with the Press-Republican's Editorial Board this way: On a strictly humanitarian level, the coverage is essential so that all — or, at least, more — of the needy are taken care of. It is unacceptable that our humane, empathetic nation would leave so much of its population without access to medicine and health care. On a financial level, getting treatment for the now-uncovered needy leads to deep and expensive health problems by the time they reach their 65th birthday. Getting them treated early would relieve a lot of that cost.
He admits that the specific figures haven't been calculated yet, but that final reckoning has to figure prominently into any argument over extending Medicare coverage.
Closing a Medicaid coverage gap that now exists between annual drug costs of between $2,700 and $6,154. Below $2,700 and above $6,154, patients can receive subsidies. Between them, there is nothing. AARP wants the government close what is known as this non-coverage "doughnut hole."
Lowering drug costs through generic biologics. Biologic drugs, used against our most serious diseases, are also our most expensive. According to Ferris, the Food and Drug Administration now has no authority to grant approval for less-expensive generics.
Offering a follow-up care benefit to prevent costly hospital readmissions.
Developing a system of long-term care wherein patients are encouraged and enabled to live at home rather than in nursing homes.
Increasing availability of low-cost care, not just for the elderly but for low-income patients, as well — extending medical benefits to Medicaid recipients, of whom there are 28,000 in Clinton, Essex and Franklin counties now, according to Erin K. Mitchell, AARP associate state director.
AARP says some of the huge outlay of money could become.......read all of the Great ideas, but what's the cost
Sunday, July 12, 2009
Can Alzheimer's Be Cured?
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Scientific American
P. Murali Doraiswamy discusses recent breakthroughs in diagnosing Alzheimer's disease and what everyone can do to postpone the onset of memory loss
P. Murali Doraiswamy is the head of biological psychiatry at Duke University and is a Senior Fellow at Duke’s Center for the Study of Aging. He’s also the co-author of The Alzheimer’s Action Plan, a guide for patients and family members struggling with the disease. Mind Matters editor Jonah Lehrer chats with Doraiswamy about recent advances in Alzheimer’s research and what people can do to prevent memory loss.
LEHRER: What do you think are the biggest public misconceptions of Alzheimer's disease?
DORAISWAMY: The two biggest misconceptions are “It’s just aging” and “It’s untreatable, so we should just leave the person alone.” Both of these misconceptions are remnants of an outdated view that hinders families from getting the best diagnosis and best care. They were also one of the main reasons I wanted to write this book.
Although old age is the single biggest risk for dementia, Alzheimer’s is not a normal part of aging. Just ask any family member who has cared for a loved one with Alzheimer’s and they will tell you how different the disease is from normal aging. Alzheimer’s can strike people as young as their forties; there are some half a million individuals in the United States with early-onset dementia. Recent research has pinpointed disruptions in specific memory networks in Alzheimer’s patients, such as those involving the posteromedial cortex and medial temporal lobe, that appear distinct from normal aging.
The larger point is that while Alzheimer’s is still incurable it’s not untreatable. There are four FDA-approved medications available for treating Alzheimer symptoms and many others in clinical trials. Strategies to enhance general brain and mental wellbeing can also help people with Alzheimer’s. That’s why early detection is so important.
LEHRER: Given the rapid aging of the American population - by 2050, the Alzheimer's Association estimates there will be a million new cases annually - what are the some preventative steps that people can take to prevent or delay the onset of the disease?
DORAISWAMY: Unfortunately, there isn’t yet a magic bullet for prevention. You can pop the most expensive anti-aging pills, drink the best red wine, and play all the brain games that money can buy, and you still might get Alzheimer’s. While higher education is clearly protective, even Nobel Laureates have been diagnosed with the disease, although it’s likely their education helped them stave off the symptoms for a little bit.
My approach is more pragmatic - it’s about recognizing risks and designing your own brain health action plan. The core of our program is to teach people about the growing links between cardiovascular markers (blood pressure, blood sugar, body weight and BMI, blood cholesterol, C-reactive protein) and brain health. A population study from Finland has developed a fascinating scale that can predict 20-year risk for dementia – sort of a brain aging speedometer. Obesity, smoking, lack of physical activity, high blood pressure, and high cholesterol are some of the culprits this study identified. So keeping these....read all of Can Alzheimer's Be Cured?
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Scientific American
P. Murali Doraiswamy discusses recent breakthroughs in diagnosing Alzheimer's disease and what everyone can do to postpone the onset of memory loss
P. Murali Doraiswamy is the head of biological psychiatry at Duke University and is a Senior Fellow at Duke’s Center for the Study of Aging. He’s also the co-author of The Alzheimer’s Action Plan, a guide for patients and family members struggling with the disease. Mind Matters editor Jonah Lehrer chats with Doraiswamy about recent advances in Alzheimer’s research and what people can do to prevent memory loss.
LEHRER: What do you think are the biggest public misconceptions of Alzheimer's disease?
DORAISWAMY: The two biggest misconceptions are “It’s just aging” and “It’s untreatable, so we should just leave the person alone.” Both of these misconceptions are remnants of an outdated view that hinders families from getting the best diagnosis and best care. They were also one of the main reasons I wanted to write this book.
Although old age is the single biggest risk for dementia, Alzheimer’s is not a normal part of aging. Just ask any family member who has cared for a loved one with Alzheimer’s and they will tell you how different the disease is from normal aging. Alzheimer’s can strike people as young as their forties; there are some half a million individuals in the United States with early-onset dementia. Recent research has pinpointed disruptions in specific memory networks in Alzheimer’s patients, such as those involving the posteromedial cortex and medial temporal lobe, that appear distinct from normal aging.
The larger point is that while Alzheimer’s is still incurable it’s not untreatable. There are four FDA-approved medications available for treating Alzheimer symptoms and many others in clinical trials. Strategies to enhance general brain and mental wellbeing can also help people with Alzheimer’s. That’s why early detection is so important.
LEHRER: Given the rapid aging of the American population - by 2050, the Alzheimer's Association estimates there will be a million new cases annually - what are the some preventative steps that people can take to prevent or delay the onset of the disease?
DORAISWAMY: Unfortunately, there isn’t yet a magic bullet for prevention. You can pop the most expensive anti-aging pills, drink the best red wine, and play all the brain games that money can buy, and you still might get Alzheimer’s. While higher education is clearly protective, even Nobel Laureates have been diagnosed with the disease, although it’s likely their education helped them stave off the symptoms for a little bit.
My approach is more pragmatic - it’s about recognizing risks and designing your own brain health action plan. The core of our program is to teach people about the growing links between cardiovascular markers (blood pressure, blood sugar, body weight and BMI, blood cholesterol, C-reactive protein) and brain health. A population study from Finland has developed a fascinating scale that can predict 20-year risk for dementia – sort of a brain aging speedometer. Obesity, smoking, lack of physical activity, high blood pressure, and high cholesterol are some of the culprits this study identified. So keeping these....read all of Can Alzheimer's Be Cured?
Friday, July 10, 2009
Popular Alzheimer’s theory may be false trail
Insider
College of Medicine
Florida University
By John Pastor
Category: From the Lab, Neuroscience
The idea that anti-inflammatory drugs might protect people struggling with dementia from Alzheimer’s disease has received a blow with the online release of a study of human brain tissue in Acta Neuropathologica.
Researchers with the McKnight Brain Institute of the University of Florida, in collaboration with scientists at the University of Frankfurt, Germany, discovered that inflammation of microglia — an abundant cell type that plays an important supporting role in the brain — does not appear to be associated with dementia in Alzheimer’s disease.
The finding supports recent clinical trial results that indicate anti-inflammatory drugs are not effective at fighting dementia in patients with Alzheimer’s disease, which affects about 5.3 million Americans.
“For almost 20 years now, it’s been claimed that brain inflammation contributes to the development of Alzheimer’s disease dementia, and based on that claim, numerous clinical trials with anti-inflammatory drugs have been conducted. They have been unsuccessful,” said Wolfgang Streit, Ph.D., a professor of neuroscience at the College of Medicine. “In the current paper we have shown that the brain’s immune system, made up of microglia, is not activated in the brains of Alzheimer’s patients, as would be the case if there were inflammation. Instead, microglia are degenerating. We claim that a loss of microglial cells contributes to the loss of neurons, and thus to the development of dementia.”
Microglial cells are a subset of a very large population of brain cells known as glial cells. Neurons are the workhorse cells of the brain, enabling thought and movement, but glia are their faithful sidekicks, providing physical and nutritional support.
Glial cells, which outnumber neurons 10-to-1, are at the heart of a popular explanation for Alzheimer’s disease that suggests protein fragments called beta amyloid — Abeta for short — clump together in the spaces between brain cells, causing memory loss and dementia. Inflammation theories suggest that microglia become “activated” and mount an immune response to these protein clumps, and instead of being helpful, a toxic release of chemicals occurs, worsening the disease effects.
However, Streit’s high-resolution observations did not find evidence that Abeta activates, or inflames, human microglia cells. Nor did researchers find evidence that inflammation is to blame for brain cell death.
“This paper potentially represents a paradigm shift in the way we look at Alzheimer’s disease,” said Mark A. Smith, Ph.D., a professor of pathology at Case Western Reserve University and editor-in-chief of the Journal of Alzheimer’s Disease. “The study goes against the very popular idea of neuro-inflammation; instead, the idea that microglia are senescent is consistent with a number of features of the disease.
“The research makes a very good case that these cells are subject to aging,” said Smith, who did not participate in the study. “These cells were thought to be activated (against Alzheimer’s), but this paper makes a strong case that they are not. The study has taken a novel approach that has led to a novel insight.”
Using a commercially available antibody, Streit for the first time created a marker for microglial cells in human brain specimens that had been in chemical storage. The specimens were from 19 people with varying degrees of Alzheimer’s, ranging from severe to none at all. Two of the samples were from Down syndrome patients, who are known to develop Alzheimer’s pathology in middle age.
When researchers examined these cells alongside neurons under a high-resolution microscope, they found that — unless an infection had occurred elsewhere in the body — microglial cells from Alzheimer’s patients were not distinctly larger or unusually shaped, which would have been the case had they been inflamed.
“What I expected to see is activated microglia right next to dying neurons,” Streit said. “That is what I did not find. What I propose is glia are dying, and the neurons lose support. We now need to find out what caused glia to degenerate. Rather than trying to find ways to inhibit microglia with anti-inflammatory drugs, we need to find ways to keep them alive and strong. It’s a whole new field.”
The microglial cells had a tangled, fragmented appearance, similar to neurons in the throes of Alzheimer’s disease or — old age.
“These cells are breaking into pieces,” said Streit, who collaborated with Alzheimer’s researcher Heiko Braak, M.D, of the Institute for Clinical Neuroanatomy in Frankfurt. “They are on their way out. For the first time, we are proving that microglial cells are subject to aging and may undergo degeneration, and that the loss of these cells precedes the loss of neurons. Research has been so focused on finding activated microglia, no one considered that these cells were degenerating and neurons lost support.”
The work was supported by.........read all of Alzheimer's theory false trial
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
College of Medicine
Florida University
By John Pastor
Category: From the Lab, Neuroscience
The idea that anti-inflammatory drugs might protect people struggling with dementia from Alzheimer’s disease has received a blow with the online release of a study of human brain tissue in Acta Neuropathologica.
Researchers with the McKnight Brain Institute of the University of Florida, in collaboration with scientists at the University of Frankfurt, Germany, discovered that inflammation of microglia — an abundant cell type that plays an important supporting role in the brain — does not appear to be associated with dementia in Alzheimer’s disease.
The finding supports recent clinical trial results that indicate anti-inflammatory drugs are not effective at fighting dementia in patients with Alzheimer’s disease, which affects about 5.3 million Americans.
“For almost 20 years now, it’s been claimed that brain inflammation contributes to the development of Alzheimer’s disease dementia, and based on that claim, numerous clinical trials with anti-inflammatory drugs have been conducted. They have been unsuccessful,” said Wolfgang Streit, Ph.D., a professor of neuroscience at the College of Medicine. “In the current paper we have shown that the brain’s immune system, made up of microglia, is not activated in the brains of Alzheimer’s patients, as would be the case if there were inflammation. Instead, microglia are degenerating. We claim that a loss of microglial cells contributes to the loss of neurons, and thus to the development of dementia.”
Microglial cells are a subset of a very large population of brain cells known as glial cells. Neurons are the workhorse cells of the brain, enabling thought and movement, but glia are their faithful sidekicks, providing physical and nutritional support.
Glial cells, which outnumber neurons 10-to-1, are at the heart of a popular explanation for Alzheimer’s disease that suggests protein fragments called beta amyloid — Abeta for short — clump together in the spaces between brain cells, causing memory loss and dementia. Inflammation theories suggest that microglia become “activated” and mount an immune response to these protein clumps, and instead of being helpful, a toxic release of chemicals occurs, worsening the disease effects.
However, Streit’s high-resolution observations did not find evidence that Abeta activates, or inflames, human microglia cells. Nor did researchers find evidence that inflammation is to blame for brain cell death.
“This paper potentially represents a paradigm shift in the way we look at Alzheimer’s disease,” said Mark A. Smith, Ph.D., a professor of pathology at Case Western Reserve University and editor-in-chief of the Journal of Alzheimer’s Disease. “The study goes against the very popular idea of neuro-inflammation; instead, the idea that microglia are senescent is consistent with a number of features of the disease.
“The research makes a very good case that these cells are subject to aging,” said Smith, who did not participate in the study. “These cells were thought to be activated (against Alzheimer’s), but this paper makes a strong case that they are not. The study has taken a novel approach that has led to a novel insight.”
Using a commercially available antibody, Streit for the first time created a marker for microglial cells in human brain specimens that had been in chemical storage. The specimens were from 19 people with varying degrees of Alzheimer’s, ranging from severe to none at all. Two of the samples were from Down syndrome patients, who are known to develop Alzheimer’s pathology in middle age.
When researchers examined these cells alongside neurons under a high-resolution microscope, they found that — unless an infection had occurred elsewhere in the body — microglial cells from Alzheimer’s patients were not distinctly larger or unusually shaped, which would have been the case had they been inflamed.
“What I expected to see is activated microglia right next to dying neurons,” Streit said. “That is what I did not find. What I propose is glia are dying, and the neurons lose support. We now need to find out what caused glia to degenerate. Rather than trying to find ways to inhibit microglia with anti-inflammatory drugs, we need to find ways to keep them alive and strong. It’s a whole new field.”
The microglial cells had a tangled, fragmented appearance, similar to neurons in the throes of Alzheimer’s disease or — old age.
“These cells are breaking into pieces,” said Streit, who collaborated with Alzheimer’s researcher Heiko Braak, M.D, of the Institute for Clinical Neuroanatomy in Frankfurt. “They are on their way out. For the first time, we are proving that microglial cells are subject to aging and may undergo degeneration, and that the loss of these cells precedes the loss of neurons. Research has been so focused on finding activated microglia, no one considered that these cells were degenerating and neurons lost support.”
The work was supported by.........read all of Alzheimer's theory false trial
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Thursday, July 9, 2009
Greater Language Skills in 20s May Guard Against Alzheimer's
US News and World Report
Small study found women who wrote more articulate essays were protected from symptoms
By Amanda Gardner
HealthDay Reporter
WEDNESDAY, July 8 (HealthDay News) -- Women with greater language abilities in early adulthood were less likely to have Alzheimer's disease later in life, even when autopsies revealed the clear brain changes that are hallmarks of the disease.
Also, the brains of women without symptoms of Alzheimer's housed bigger neurons, according to a study appearing in the July 9 online edition of Neurology.
"We noticed that the neurons in this group of people are larger and we also know that the same group of people we call asymptomatic also had higher language skills during their 20s," said study author Dr. Diego Iacono, a research fellow in neuropathology at Johns Hopkins University in Baltimore.
It's possible that the larger neurons compensated for the brain plaques and tangles that are usually indicative of Alzheimer's, the authors stated.
The findings could also mean that language abilities in the early 20s can predict the risk of developing dementia several decades later.
A previous study, this one in men, also found larger neurons in individuals who had plaques and tangles but no clinical evidence of Alzheimer's.
For the current study, researchers examined the brains of 38 deceased Catholic nuns, part of the ongoing Nun Study.
Women were divided into two groups: those with symptoms of memory loss along with plaques and tangles and those with no memory loss whether or not they had plaques or tangles.
Essays written by the women when they first entered the convent in their late teens or early 20s were analyzed for richness of language skills, including how many ideas were expressed per 10 words, number of verbs and adjectives in one sentence and more.
Women without memory problems scored......read all of Greater Language Skills in 20s May Guard Against Alzheimer's
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Small study found women who wrote more articulate essays were protected from symptoms
By Amanda Gardner
HealthDay Reporter
WEDNESDAY, July 8 (HealthDay News) -- Women with greater language abilities in early adulthood were less likely to have Alzheimer's disease later in life, even when autopsies revealed the clear brain changes that are hallmarks of the disease.
Also, the brains of women without symptoms of Alzheimer's housed bigger neurons, according to a study appearing in the July 9 online edition of Neurology.
"We noticed that the neurons in this group of people are larger and we also know that the same group of people we call asymptomatic also had higher language skills during their 20s," said study author Dr. Diego Iacono, a research fellow in neuropathology at Johns Hopkins University in Baltimore.
It's possible that the larger neurons compensated for the brain plaques and tangles that are usually indicative of Alzheimer's, the authors stated.
The findings could also mean that language abilities in the early 20s can predict the risk of developing dementia several decades later.
A previous study, this one in men, also found larger neurons in individuals who had plaques and tangles but no clinical evidence of Alzheimer's.
For the current study, researchers examined the brains of 38 deceased Catholic nuns, part of the ongoing Nun Study.
Women were divided into two groups: those with symptoms of memory loss along with plaques and tangles and those with no memory loss whether or not they had plaques or tangles.
Essays written by the women when they first entered the convent in their late teens or early 20s were analyzed for richness of language skills, including how many ideas were expressed per 10 words, number of verbs and adjectives in one sentence and more.
Women without memory problems scored......read all of Greater Language Skills in 20s May Guard Against Alzheimer's
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Tuesday, July 7, 2009
Alzheimer's and Home Health Care Costs
Brian Willie
For many families, home health care is the way to go to take care
of their loved one with Alzheimer's. That is, at least for awhile.
There are some very good home health care providers, but they can
be very expensive. The average cost is $16-24/hour. For the family
that needs moderate levels of help, this may not be bad, but as
care needs increase, and more and more hours must be spent on home
health care, the Alzheimer's family will face tremendous expenses.
I recently met with someone who runs a home health service and she
told me that it's not uncommon for round the clock care to cost as
much as $3,600 a week!
We will talk more about how a little known Veteran's Benefit can
often be used to offset some of the tremendous costs of home health
for your loved one with Alzheimer's.
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Monday, July 6, 2009
New triggers found for Alzheimer's
Tom Blackwell, National Post
For decades, scientists have struggled to understand what causes Alzheimer's disease, once even suspecting that exposure to aluminum pots and pans played a role. Much is still unknown.
New Canadian research, however, offers a novel clue, concluding that infectious diseases such as bacterial pneumonia and the virus behind cold sores may make people more susceptible to the devastating illness - and indicate a way to guard against Alzheimer's.
If borne out with more study, the findings would make it even more important to aggressively treat infection, while raising the possibility that vaccines against certain bacteria or viruses could actually prevent Alzheimer's, says a paper published in the journal Alzheimer's and Dementia.
"It is kind of counter-intuitive. You think an infection is gone and that is it, right?" said Dr. Paul Verhoeff, a psychiatrist at Toronto's Baycrest brain-research facility. "But think about those cold sores. Whenever your immune system is compromised, those cold sores come back ... We think that some infections can really increase the chance someone could develop Alzheimer's if the person already has other predisposing factors."
About 500,000 Canadians suffer from Alzheimer's disease and that number is expected to double within 25 years, with women being disproportionately afflicted. The main known risk factors for the degenerative brain condition include old age, diabetes, family history and cardiovascular disease.
Dr. Verhoeff and colleagues at Toronto's Sunnybrook Health Sciences Centre reviewed several studies conducted over the last decade or so that explored a link between various infections and Alzheimer's.
The most convincing evidence involves Chlamydia pneumoniae, a common bacteria estimated to be present in more than half of American adults and to cause 10-20% of the pneumonia cases outside of hospital.
One autopsy-based study found the bug in the brains of 90% of 19 Alzheimer's patients, and in just 5% of the brains of non-Alzheimer's subjects. Another detected the bacteria located close to the amyloid plaques considered a hallmark of Alzheimer's brains.
The C. pneumoniae microbe does not appear to cause the disease, but may make people more vulnerable to it and accelerate the progress of Alzheimer's, the researchers concluded.
Other studies have unearthed a link between the Herpes simplex virus - another widespread bug that causes cold sores - and Alzheimer's in people with APOE-4, a gene that itself is a risk factor for the disease.
How those and other infections might speed on the onset of Alzheimer's is unclear, but is likely related to the inflammatory effects of the pathogens, Dr. Verhoeff said.
It could be that treating infection will one day help.......read all of New triggers found for Alzheimer's
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
For decades, scientists have struggled to understand what causes Alzheimer's disease, once even suspecting that exposure to aluminum pots and pans played a role. Much is still unknown.
New Canadian research, however, offers a novel clue, concluding that infectious diseases such as bacterial pneumonia and the virus behind cold sores may make people more susceptible to the devastating illness - and indicate a way to guard against Alzheimer's.
If borne out with more study, the findings would make it even more important to aggressively treat infection, while raising the possibility that vaccines against certain bacteria or viruses could actually prevent Alzheimer's, says a paper published in the journal Alzheimer's and Dementia.
"It is kind of counter-intuitive. You think an infection is gone and that is it, right?" said Dr. Paul Verhoeff, a psychiatrist at Toronto's Baycrest brain-research facility. "But think about those cold sores. Whenever your immune system is compromised, those cold sores come back ... We think that some infections can really increase the chance someone could develop Alzheimer's if the person already has other predisposing factors."
About 500,000 Canadians suffer from Alzheimer's disease and that number is expected to double within 25 years, with women being disproportionately afflicted. The main known risk factors for the degenerative brain condition include old age, diabetes, family history and cardiovascular disease.
Dr. Verhoeff and colleagues at Toronto's Sunnybrook Health Sciences Centre reviewed several studies conducted over the last decade or so that explored a link between various infections and Alzheimer's.
The most convincing evidence involves Chlamydia pneumoniae, a common bacteria estimated to be present in more than half of American adults and to cause 10-20% of the pneumonia cases outside of hospital.
One autopsy-based study found the bug in the brains of 90% of 19 Alzheimer's patients, and in just 5% of the brains of non-Alzheimer's subjects. Another detected the bacteria located close to the amyloid plaques considered a hallmark of Alzheimer's brains.
The C. pneumoniae microbe does not appear to cause the disease, but may make people more vulnerable to it and accelerate the progress of Alzheimer's, the researchers concluded.
Other studies have unearthed a link between the Herpes simplex virus - another widespread bug that causes cold sores - and Alzheimer's in people with APOE-4, a gene that itself is a risk factor for the disease.
How those and other infections might speed on the onset of Alzheimer's is unclear, but is likely related to the inflammatory effects of the pathogens, Dr. Verhoeff said.
It could be that treating infection will one day help.......read all of New triggers found for Alzheimer's
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Sunday, July 5, 2009
Ultimate Alzheimer's Care Rescue Program: Spots Filling Up Fast
Brian Willie
Here is a special offer you should not miss if you are caring for a loved one with Alzheimer's disease or a related dementia.
Brian Willie
Elder Law Attorney
Here we are on July 5th (is th...and
all around the U.S. we enjoyed our
Independence Day with hotdogs, apple pie & fireworks!
This is the perfect chance to think
about your independence.
It's also the perfect chance to celebrate the re-release of my "Ultimate Alzheimer's
Care Rescue Program."
You may remember that I released this a few months back, and it literally sold
out in less than a week.
Well, I've decided to open up the doors, and as a special Independence Day
incentive, you can pick up a copy of my program at its OLD introductory price.
But, this will not last. Starting next week, the price is going up significantly
and I'm releasing it to the general public.
So claim a copy of this 6 set audio program with full transcripts for
yourself.
ultimate alzheimers rescue program
This program is life-changing. It's comprehensive, factual and easy
to understand. And, it will finally give you that "ah ha" moment
where it all comes together.
And, the information is delivered using audio recordings that you
can easily listen to right on your computer, (just push play)
or even put it onto a cd or ipod if you like.
You'll also be able to just click on the transcripts that go along
with each module and follow right along.
So all you'll have to do is relax and listen as I walk you through
each part in hand-holding style.
But-a quick word to the wise: I have to limit the number I release,
so that I can focus on you and your individual needs.
And, the price is heading up next week.
Since I have ALOT of people who receive my emails and newsletter and an
almost frenzy of people on my priority notice list that have
already received this, you do have to act fast.
The decision to move forward, or not, will have a big impact on
your family's life. It may mean the difference between running out
of money after less than 26 weeks of long-term care or having a
nice nest egg for your family.
All the best!
Brian Willie
Elder Law Attorney
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
They are happy they used the ultimate alzheimers rescue program
Here is a special offer you should not miss if you are caring for a loved one with Alzheimer's disease or a related dementia.
Brian Willie
Elder Law Attorney
Here we are on July 5th (is th...and
all around the U.S. we enjoyed our
Independence Day with hotdogs, apple pie & fireworks!
This is the perfect chance to think
about your independence.
It's also the perfect chance to celebrate the re-release of my "Ultimate Alzheimer's
Care Rescue Program."
You may remember that I released this a few months back, and it literally sold
out in less than a week.
Well, I've decided to open up the doors, and as a special Independence Day
incentive, you can pick up a copy of my program at its OLD introductory price.
But, this will not last. Starting next week, the price is going up significantly
and I'm releasing it to the general public.
So claim a copy of this 6 set audio program with full transcripts for
yourself.
ultimate alzheimers rescue program
This program is life-changing. It's comprehensive, factual and easy
to understand. And, it will finally give you that "ah ha" moment
where it all comes together.
And, the information is delivered using audio recordings that you
can easily listen to right on your computer, (just push play)
or even put it onto a cd or ipod if you like.
You'll also be able to just click on the transcripts that go along
with each module and follow right along.
So all you'll have to do is relax and listen as I walk you through
each part in hand-holding style.
But-a quick word to the wise: I have to limit the number I release,
so that I can focus on you and your individual needs.
And, the price is heading up next week.
Since I have ALOT of people who receive my emails and newsletter and an
almost frenzy of people on my priority notice list that have
already received this, you do have to act fast.
The decision to move forward, or not, will have a big impact on
your family's life. It may mean the difference between running out
of money after less than 26 weeks of long-term care or having a
nice nest egg for your family.
All the best!
Brian Willie
Elder Law Attorney
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
They are happy they used the ultimate alzheimers rescue program
Saturday, July 4, 2009
Researchers study connection between cataracts and dementia
wkyc.com
Cleveland/Akron Ohio
A team of researchers, led by the Mandel School of Applied Social Sciences at Case Western Reserve University, will begin a five-year, $2.9 million National Institutes of Health-funded study.
They will examine the lives of patients with both cataracts and Alzheimer's disease (AD) to see if restored vision improves everyday life for people with dementia.
Grover "Cleve" Gilmore, dean of the Case Western Reserve Mandel School and principal investigator of the study says in 20 years of research, he's found people with dementia lose their ability to see objects in medium- and low-contrast environments, but boosting the contrast of objects improves their ability to move around their homes; eat better; read; and do other simple, everyday tasks.
Cataracts cloud and blur the vision in the eye causing AD patients additional problems. If untreated...........read all of Researchers study connection between cataracts and dementia
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Cleveland/Akron Ohio
A team of researchers, led by the Mandel School of Applied Social Sciences at Case Western Reserve University, will begin a five-year, $2.9 million National Institutes of Health-funded study.
They will examine the lives of patients with both cataracts and Alzheimer's disease (AD) to see if restored vision improves everyday life for people with dementia.
Grover "Cleve" Gilmore, dean of the Case Western Reserve Mandel School and principal investigator of the study says in 20 years of research, he's found people with dementia lose their ability to see objects in medium- and low-contrast environments, but boosting the contrast of objects improves their ability to move around their homes; eat better; read; and do other simple, everyday tasks.
Cataracts cloud and blur the vision in the eye causing AD patients additional problems. If untreated...........read all of Researchers study connection between cataracts and dementia
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Friday, July 3, 2009
David Holtzman: Attacking Alzheimer's With a New Test for Amyloid Beta
USNews.com
His SILK test quickly reveals whether medication is working to limit the harmful protein amyloid beta
By January W. Payne
Neuroscientist David Holtzman was captivated by Alzheimer's disease as a medical student. Now the 47-year-old associate director of the Alzheimer's Disease Research Center at the Washington University School of Medicine in St. Louis, Holtzman says he realized that Alzheimer's "was going to be one of the biggest problems that we would face, and it was unsolved." Figuring out how the illness begins and how to prevent or slow it has been his goal ever since.
Holtzman's persistence is paying off. Until now, it typically took about two years to determine whether a new Alzheimer's drug was having an effect. But recently, he and colleagues devised a test that rapidly shows whether an experimental medication has a chance of working. "There aren't good ways without doing a long, expensive trial" to determine this, he says. But with the new test, called stable isotope-linked kinetics, or SILK, "we were able to come up with a technique to figure out over a day or two whether a drug is hitting its target in the brain," he says.
SILK reveals whether the.......read all of Attacking Alzheimer's With a New Test for Amyloid Beta
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
His SILK test quickly reveals whether medication is working to limit the harmful protein amyloid beta
By January W. Payne
Neuroscientist David Holtzman was captivated by Alzheimer's disease as a medical student. Now the 47-year-old associate director of the Alzheimer's Disease Research Center at the Washington University School of Medicine in St. Louis, Holtzman says he realized that Alzheimer's "was going to be one of the biggest problems that we would face, and it was unsolved." Figuring out how the illness begins and how to prevent or slow it has been his goal ever since.
Holtzman's persistence is paying off. Until now, it typically took about two years to determine whether a new Alzheimer's drug was having an effect. But recently, he and colleagues devised a test that rapidly shows whether an experimental medication has a chance of working. "There aren't good ways without doing a long, expensive trial" to determine this, he says. But with the new test, called stable isotope-linked kinetics, or SILK, "we were able to come up with a technique to figure out over a day or two whether a drug is hitting its target in the brain," he says.
SILK reveals whether the.......read all of Attacking Alzheimer's With a New Test for Amyloid Beta
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
Thursday, July 2, 2009
Top ten, 4th of July, activities for those with Alzheimer's disease and related dementias
Healthnrws-stat.com
Author and dementia healthcare professional,Susan Berg, suggests ways to enjoy the holiday with dementia folks that are stress and falure free.
Here are some easy, yet fun things to do on or near the 4th of July together
10. Arrange flowers real of fake. You can use red, white and blue flowers to make the bouquet or centerpiece look patriotic.
9. Plan a picnic or a party from beginning to end
8. Have a picnic perhaps using the ideas from your plans. If the person with dementia does not want to go outside, no problem, have the picnic inside.
7. Go to the beach or the park. Go at off times to avoid the crowd. You can always go on different day. Again if you fear a negative reaction to going to the beach, bring the beach to your home. Get some sand, sea shells and other beach paraphernalia.
6 Have a small get together at home. Hire or have someone to assist the ADRD person.
5. Draw some patriotic pictures. You can use paints, magic markers or crayons. Fireworks are easy to draw.
4. Read a........more of the Top ten, 4th of July, activities for those with Alzheimer's disease and related dementias
Here is a great dementia resource for caregivers and healthcare professinals,
Here is information on being the best caregiver you can be
Here are more interesting dementia articles and activities,
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