Wednesday, May 30, 2012

Successful Alzheimer's drug trial


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The Dementia Caregiver's Little Book of Hope [Kindle Edition



Reuters



 Danish drugmaker Lundbeck said patients who took its Alzheimer's drug candidate Lu AE58054 in a phase 2 clinical trial achieved statistically significant improvement in cognitive performance when the compound was added to donepezil.

Lundbeck said the clinical study in 278 patients suffering from Alzheimer's disease had achieved its main target and that Lu AE58054 was also well-tolerated in combination with donepezil.

"These results are very encouraging, and we are now evaluating how to best proceed with the development of Lu AE58054," Anders Pedersen, head of research and development at Lundbeck, said in the statement.

Lundbeck said Alzheimer's disease affects over 26 million people worldwide, and the cost to society has been reported as $600 billion per year

Monday, May 28, 2012

Smell Tests Don't Predict Alzheimer's


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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

HealthDay News

Smell tests should not be used to predict Alzheimer's disease, the most common form of dementia, according to a new study.



Although there is a link between the two, researchers found other medical problems may cause people to lose their sense of smell, and it may not necessarily mean they will develop the progressive brain disorder later in life.


"A nonspecific association between poor smell function and Alzheimer's dementia is not the same as actually being able to use a smell test to predict Alzheimer's," Dr. Gordon Sun, a general otolaryngologist at the University of Michigan in Ann Arbor, said in a university news release.


"Unfortunately, this misinterpretation of the research has led to the promotion of these tests by the media and public figures like Dr. Oz," he added. "This study helps set the record straight about where the evidence currently stands."


In conducting the comprehensive review, the study's authors examined nearly 1,200 articles dating back to 1984. Two studies that tracked patients over time and 30 studies that evaluated patients at one specific point in time met inclusion criteria.


"Understandably, researchers, clinicians and the public are eager for a simple, accurate, and inexpensive way to predict or diagnose Alzheimer's early, but we're not there yet," argued Sun, who is also a Robert Wood Johnson Foundation/U.S. Veterans Affairs Clinical Scholar at the University of Michigan Medical School.

"My concern is that by promoting smell tests at this point, we create false hope or even false alarm among seniors and their families," he said. "Additional research is needed before we can rely on smell tests to predict the later onset of Alzheimer's."


The study, published online in the journal Laryngoscope, concluded that patients visit their primary care physician if they are concerned about their risk for Alzheimer's disease.


About 5.4 million Americans have Alzheimer's disease, most of them aged 65 and older, according to the Alzheimer's Association. That number is expected to rise rapidly as the Baby Boomer generation ages.


More information


The U.S. National Institute on Aging provides more information on Alzheimer's disease.




Saturday, May 26, 2012

Brain Scan for Alzheimer's


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The Dementia Caregiver's Little Book of Hope [Kindle Edition]


Technology Review


A recently approved plaque-tracking dye can improve doctors' ability to identify Alzheimer's.


by Susan Young


Beginning next month, doctors can use a brain scan to better diagnose Alzheimer's. The U.S. Food and Drug Administration recently approved a fluorescent dye that binds to amyloid plaques, a physical hallmark of the disease, as a diagnostic tool.  


Currently, doctors cannot be certain whether or not a patient's brain is riddled with amyloid plaques until after the patient's death. But now, clinicians can use a weakly radioactive dye to search for the presence of plaques in a living patient. The dye binds to the starchy amyloid that builds up in the brains of Alzheimer's patients and can be visualized in a PET scan. The FDA approved the scan as a method for estimating plaque content in the brains of people exhibiting cognitive decline. The presence or absence of plaques in a patient with forgetfulness, confusion, or other signs of neurological trouble could help doctors with their diagnoses. 
Although scientists do not know whether or not the plaques are the cause of Alzheimer's, the plaques are strongly correlated with symptoms of dementia. Elderly people with the plaques have a more rapid mental decline than the elderly who don't have the plaques. And even though doctors cannot treat Alzheimer's, diagnostic tools like the plaque-marking dyes will help them identify patients with the disease, as well as those who do not have it but exhibit signs of mental decline due to other problems.
"A positive scan would add more weight to our bedside diagnosis," says Liana Apostolova, an Alzheimer's specialist at the University of California, Los Angeles. She says the technique could be useful in diagnosing patients with unusual forms of the disease and patients whose symptoms may be caused by other conditions, such as drug side effects or depression. "If a patient's cognitive impairment is purely due to depression, then a negative amyloid scan would help ascertain that," Apostolova says.  


The new dye and other plaque-marking dyes have been used in clinical research for years, but Eli Lily, whose subsidiary Avid Radiopharmaceuticals produces the diagnostic agent, is the first to bring the technique to the doctor's office. Some experts are still concerned that the clinical use of the dye might be a bit premature, since the presence of the plaques isn't enough to confirm an Alzheimer's diagnosis. In fact, the amyloid deposits are often found in older people with normal mental ability and could be associated with other neurologic conditions. For now, the Avid dye is only approved to be used to rule out Alzheimer's (if no plaques are detected, a doctor can be confident the patient doesn't have the disease).

"I think it puts the clinician in a bind," says Ronald Petersen, director of the Mayo Clinic's Alzheimer's Disease Research Center. If a scan is negative, then a doctor can tell a patient that amyloid is not contributing, but if a scan is positive, what should a clinician do? "The FDA nor the company says anything about the meaning of a positive scan," says Petersen. "The data is not out there."
Petersen and others agree, however, that plaque-detecting diagnostics are critical for Alzheimer's research. The dyes enable researchers to determine which participants carry plaques and thus design better trials for plaque-attacking drugs. Within the trials, plaque tracers can be used to monitor the amount of plaque in a participant's brain during the course of treatment.
The tracers can also help the field elucidate the causes and disease mechanisms of Alzheimer's, which will be key to treating or preventing the disease. Researchers can study people who have amyloid plaques and monitor their cognitive abilities over time. From the pool of cognitively normal elderly with a positive scan, knowing who "develops Alzheimer's disease and who doesn't will help us explore disease susceptibility and resistance, identify all genetic risk factors and the early metabolic changes, so we can then target these specific processes with drugs," Apostolova says. "Diagnoses can be helpful, but we want therapeutics."
More than five million people in the United States have Alzheimer's, and that number is expected to double in coming years, according to the U.S. Department of Health and Human Services. By their early 70s, as many as 30 percent of people have amyloid plaques in the brain, says Michael Weiner, principal investigator of the Alzheimer's Disease Neuroimaging Initiative, which tests imaging techniques as well as biomarkers for Alzheimer's that could be found in the blood or cerebrospinal fluid.
The new dye-based scans "are going to create greater public consciousness of the disease, and that will have a big impact," says Weiner.



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Friday, May 25, 2012

Why you should beat smoking


Health care professionals and caregivers of people with dementia and other neurological problems, here is some information you will find useful.

Smoking has been shown to be bad for all people. It affects every organ in your body in a negative way. There is nothing good about it. Yet millions of people still smoke despite the risk they put themselves at.

If you or a loved one have been a lifelong smoker, you are at a huge risk for developing dementia sooner rather than later. Of course you or a loved one may escape the clutches of dementia, but you could develop heart disease, lung cancer or kidney disease by smoking.

What is really bad is if your loved one already has dementia. There are just so many risks if he or she continues to smoke. First of all, the dementia will progress more rapidly than if he or she quit. It may be hard to get him or her to stop because he or she is so used to doing it

Also imagine the safety risk. They could easily start a fire by being careless lighting the cigarette. Or he or she could fall asleep while his or her cigarette is still burning.

If you, the caregiver, smoke, then your loved one with dementia undoubtedly will have some negative effects from the second hand smoke. So you and they need to be beating smoking before it is too late.

Thursday, May 24, 2012

USF Health part of national resveratrol study for Alzheimer’s disease


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USF

Can a component found in red wine help change the course of Alzheimer’s disease?


The USF Health Byrd Alzheimer’s Institute has been selected as one of the sites for a federally-sponsored clinical study testing whether resveratrol can alter or delay memory deterioration and daily functioning in people with mild to moderate Alzheimer’s disease.


Some of the highest levels of resveratrol are found in red wine and the skin of red grapes, but the plant-derived compound is also present in chocolate, berries, tomatoes and peanuts.


The double-blind, placebo-controlled Resveratrol for Alzheimer’s Disease Study, supported by the National Institute on Aging, will be conducted at 26 sites across the United States affiliated with the Alzheimer’s Disease Cooperative Study. Each research site, including USF’s, will enroll up to 10 participants


Amanda Smith, MD, medical director at the Byrd Alzheimer’s institute, leads the USF site study on the safety, tolerability and effectiveness of the natural compound (pure resveratrol in capsule form). The one-year trial has begun recruiting participants.


“This is an exciting study for a couple of reasons,” Dr. Smith said. “First, it is a naturally-occurring substance, and that is sometimes more appealing to participants. Secondly, it approaches the disease from a different angle than many other treatments being tested, so it could be another weapon in the multi-pronged approach to treating Alzheimer’s.”


Resveratrol activates a class of enzymes known as sirtuins, which are involved in modulating metabolism and may affect regulatory pathways of diseases of aging. Pre-clinical research and pilot clinical studies suggest the compound may prevent diabetes, ward off cardiovascular disease, act as a natural cancer fighter, and prevent memory loss, but there has been no large definitive study of its effects in humans.


“It’s a hot topic of research interest these days,” said Min You, PhD, associate professor in the USF Health Department of Molecular Pharmacology and Physiology, whose published studies of resveratrol in mice found that the substance may prevent alcoholic fatty liver disease.


“SIRT1, one of the targets of resveratrol, is a metabolic sensor in every tissue of the body, including the heart, liver and brain,” Dr. You said. “Resveratrol keeps metabolic processes in balance and plays a role in longevity.”
Dr. You, who has studied resveratrol and its regulatory pathways for nearly eight years, believes the compound may have greater potential to prevent than treat age-related diseases like Alzheimer’s, diabetes, obesity and heart disease. “It’s quickly removed from the bloodstream when consumed, so you’d likely have to take a very high amount of resveratrol to reverse pathology,” she said. “However chronic consumption of low-dose resveratrol could be good as a preventive approach.”




For more information on the Resveratrol for Alzheimer’s Disease Study, call the Byrd Institute at (813) 974-4355.









Tuesday, May 22, 2012

Alzheimer's plan and drug trials


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Medpage Today

Friday, May 18, 2012

Researchers move closer to delaying dementia


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UQ News

Scientists at UQ's Queensland Brain Institute are one step closer to developing new therapies for treating dementia.



QBI's Dr Jana Vukovic said the work was aimed at understanding the molecular mechanism that may impair learning and memory in the aging population.


“Aging slows the production of new nerve cells, reducing the brain's ability to form new memories,” said Dr Vokovic, who performed the work in the laboratory of Professor Perry Bartlett, the Director of QBI at The University of Queensland.


"But our research shows for the first time that the brain cells usually responsible for mediating immunity, microglia, have an inhibitory effect on memory during aging.


“Furthermore, they have shown that a molecule produced by nerve cells, fractalkine, can reverse this process and stimulate stem cells to produce new neurons.”


The discovery, published in The Journal of Neuroscience today, came after QBI scientists observed that the increased production of new neurons in mice that were actively running was due to the release of fractalkine in the hippocampus – the brain structure responsible for specific types of learning and memory.

Professor Bartlett said it had been known for some time that exercise increased the production of new nerve cells in the hippocampus in young and even aged mice.

“But this study found that it is fractalkine that appears to be specifically mediating this effect by making the microglia produce factors that activate the stem cells that produce new nerve cells,” he said.

“Once the cells are activated they divide and produce new cells, which underpin the animal's ability to learn and form memories.



"This means that fractalkine may form the basis for the development of future therapies.

“The discovery is especially exciting because we have found that older animals suffering cognitive decline showed significantly lower levels of fractalkine.

“We are seeking ways of increasing fractalkine levels in patients with cognitive decline, and hoping this may be a new frontline therapy in treating dementia.”


Dr Vukovic said that until relatively recently, it was thought the adult brain was incapable of generating new neurons.

“But work from Professor Bartlett's laboratory over the past 20 years has demonstrated that the brains of adult animals, including humans, retain the ability to make new nerve cells,” she said.


“The challenge is to find out how to stimulate this production in the aged animal and human where production has slowed.”

The latest work was a significant step toward achieving this goal, she said.


The article published today is titled Microglia modulate hippocampal neural precursor activity in response to exercise and aging. Its authors are Jana Vukovic, Michael J. Colditz, Daniel G. Blackmore, Marc J. Ruitenberg, Perry F. Bartlett




Wednesday, May 16, 2012

Study Links Depression And Dementia


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Huffington Post

People who suffer from chronic depression throughout their lives are more likely to develop dementia compared with people who aren't depressed, according to a study released Monday.


The study, by California researchers, sheds light on whether depression might cause dementia and Alzheimer's disease, or if it is merely an early sign of memory loss and other problems associated with dementia. Alzheimer's disease is the leading cause of dementia; the second-leading cause is impaired blood supply to the brain, resulting in what is known as vascular dementia

"It's quite clear depression late in life can be an early sign of Alzheimer's," explained Rachel Whitmer, a study researcher and an investigator at the Kaiser Permanente Northern California Division of Research. "There's a lot of debate whether [depression] is really a risk factor for dementia, or if it just shows up."

The findings, published in the May issue of Archives of General Psychiatry, add to the evidence that late-in-life depression is a likely early sign of Alzheimer's disease and suggest that chronic depression appears to increase the risk of developing vascular dementia. Adequate treatment for depression in midlife could cut the risk of developing dementia. The study is the first to examine whether midlife or late-life depression is more likely to lead to either Alzheimer's disease or vascular dementia over the long term.


To look at links between depression and dementia, Dr. Whitmer and other researchers looked at 13,535 long-term Kaiser Permanente members who had enrolled in a larger study in the period from 1964 to 1973 at ages ranging from 40 to 55 years old. Health information, including a survey that asked about depression, was collected at the time.

Researchers looked at whether the same people were depressed late in life, in the period from 1994 to 2000, and then looked at whether they were diagnosed with dementia or Alzheimer's disease in 2003. The participants' average age in 2003 was 81 and 57.9% were women. The study found depression present in 14.1% of subjects in midlife only, in 9.2% in late life only and in 4.2% in both
Looking at those who later developed dementia, the study found 20.7% of study participants without depression developed dementia, compared with 23.5% of people who reported depression in midlife only and 31.4% of those who were depressed later in life. Among those who were depressed at both mid- and late-life, 31.5% developed dementia.
Researchers then did more analysis to tease out Alzheimer's diagnoses from the broader dementia category. They found people who were depressed in midlife but not late in life had no increased risk of developing Alzheimer's disease or vascular dementia. People who were depressed late in life were more likely to develop Alzheimer's while those depressed at both mid- and late life were three times as likely to develop vascular dementia.

Dr. Whitmer's research focused on people's health and how it affects brain aging. Previous studies she has conducted using Kaiser's database of long-term members, have shown that factors such as smoking, diabetes, high cholesterol and belly fat increase the risk of developing Alzheimer's and other brain diseases. A 2008 study looking at belly fat showed people who had more belly fat during middle age had higher rates of dementia when they reached old age. The finding held true even for people whose overall body weight was considered normal.




Monday, May 14, 2012

Mitochondria Dysfunction Occurs Early in Alzheimer’s Disease Prior to Memory Loss, Amyloid Deposits

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Highlight health

Walter  Jessen
Mitochondria are specialized subunits inside a cell that produce the cell’s energy and regulate its metabolism. Research suggests that mitochondria may play a central role in neuronal cell survival because they regulate both energy metabolism and cell death pathways. Using genetic mouse models of Alzheimer’s disease, researchers from Mayo Clinic have found that mitochondria in the brain are dysfunctional early in the disease. The findings were recently published in the open access journal PLoS ONE.

Using real time imaging, scientists examined mitochondria in live neurons from three different mouse models of Alzheimer’s disease. Each of the mouse models had a different gene mutation shown to cause familial, or early-onset, Alzheimer’s disease. To evaluate the the impact of a given mutation, mitochondrial motility, distribution, ultrastructure and function in neurons and brain tissue was examined early in mouse development until the age where mice began to display memory loss and amyloid deposits formed.

Researchers used a mitochondria-specific dye and monitored axonal trafficking (i.e. motion along axons or nerve fibers). The investigators found that mitochondrial axonal trafficking is inhibited in embryonic neurons afflicted with Alzheimer’s disease, well before mice showed any memory loss or amyloid plaque formation.


Indeed, inhibition of axonal trafficking was found to be a general defect that occurred in all three mouse models of Alzheimer’s disease and was not specific for mitochondria. Nevertheless, neurons with inhibited mitochondrial trafficking were found to be more susceptible to excitotoxic cell death, a pathological process wherein nerve cells are killed by excessive neurotransmitter stimulation.
In the brains of all three mouse models of Alzheimer’s disease, mitochondria tended to lose their integrity and subsequently stopped functioning. Importantly, dysfunctional mitochondria were detected at the synapses of neurons involved in maintaining memory, suggesting a direct linkage with Alzheimer’s disease.


The scientists also applied a method called metabolomics, which measures the chemical fingerprints of specific metabolic pathways in the cell such as sugars, lipids, nucleotides, amino acids and fatty acids. The approach takes a snapshot of what is happening in the body at a given time and at a hight level of detail, and provides insight into the cellular processes that underlie a disease. For this study, the metabolomic profiles showed changes in metabolites related to mitochondrial function and cellular energy metabolism, which further confirmed that altered mitochondrial energetics is fundamental to the disease process.
The researchers identified a panel of metabolomic biomarkers. According to Eugenia Trushina, Ph.D., Mayo Clinic pharmacologist and senior investigator on the study [2]:


We are not looking at the consequences of Alzheimer’s disease, but at very early events and molecular mechanisms that lead to the disease. We expect to validate metabolomic changes in humans with Alzheimer’s disease and to use these biomarkers to diagnose the disease before symptoms appear — which is the ideal time to start treatment.

The researchers conclude by stating that Alzheimer’s disease can be viewed as a mitochondrial movement disorder with evolving energetic deficit represented by the panel of metabolomic biomarkers and that mitochondrial dysfunction is an underlying event in Alzheimer’s disease progression.
References


1.Trushina et al. Defects in mitochondrial dynamics and metabolomic signatures of evolving energetic stress in mouse models of familial Alzheimer’s disease. PLoS One. 2012;7(2):e32737. Epub 2012 Feb 29.



2.Mitochondrial Dysfunction Present Early in Alzheimer’s, Before Memory Loss. Mayo Clinic News. 2012 Feb 29.

Saturday, May 12, 2012

What to do about a neurlogical disorder

Health care professionals and persons in charge of the care of a person with a brain disorder, here is some information that will be useful to you.

There are instances that you may need to consult a Neurology Specialist. There is an oustanding medical center in New York that has a state of the art neurology department. Perhaps your patient or loved has dementia.

They may have adult epilepsy which caused brain damage leading to dementia. You will want to try to avoid brain damage so it is best to consult an Epilepsy Specialist to help avoid any kind of brain damage. There is a great place in New York which people from all over the world travel to.Also Beth Israel in New York has many subspecialties in neurology if there is another issue.

If brain damage occurred because of epilepsy or another neurological disorder, you will want to keep the persons’ brain as active as possible to minimize their mental decline.


Try to pinpoint some areas of mental strength and devise activities that focus on these areas. Music is a great tool to introduce to people because it uses so many areas of the brain. People seem to remember the words and melodies to songs when they may remember nothing else.

It is best to use trial and error to see what songs they respond to. It may be songs from the past or it may be other songs.

If you do this in combination with the use of a Neurology Specialist, you will get the best results possible. Whether your patient, client or loved one has adult epilepsy, or another neurology deficit resulting in dementia, this is the best option.



What can a Neurology Specialist do for your patient, client or loved one? They are people who are considered to be experts in problems with the brain and thinking skills. They are able to diagnose problems that may otherwise go undetected because of their knowledge and skill level. So as I stated previously, consult a Neurology Specialist and devise some activities to keep the brain active.




Why is laughter the best medicine

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Psych Central

What happens during laughter? It has to do with breathing, as neuroscientist Sophie Scott explains, as well as emotions, and the voice. Studying the mechanisms of laughter, she discovered it’s a social, universal expression in all people including those with dementia and not just in humans but even chimpanzees and rats. Brain scans revealed the areas of the brain active during laughter (interestingly, similar to yawning, another socially contagious expression). Her lab also examined polite, posed laughter vs. uncontrollable mirth, and revealed how we tell the difference

Thursday, May 10, 2012

Breaking the News That a Loved One is Going on Hospice Care

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Author, columnist and speaker Carol Bradley Bursack

When the paperwork was finally signed to get hospice care for my dad, I was grateful. There would now be a routine of care for him where he could live in comfort. That's all he really wanted. However, I knew that breaking this news to Mom would be difficult. She'd have to finally admit, and somehow accept, the fact that Dad was dying. After all, hospice care is for people diagnosed as terminally ill.



A brief time after Dad's death, Mom's own terminal condition required hospice care in order to control her pain. She had told me numerous times that she was tired of living and ready to "go." Yet, I believe it still was hard for her to accept that she needed hospice care and what that meant.


Our culture has historically been devoted to cure illness at all costs, and death is often looked at as "failure," no matter the age or condition of the person being treated. Many other cultures readily accept death as part of the life cycle. I believe we, as a culture, are making progress in this direction, but death still tends to be a word people avoid. If it's up to you to inform a loved one that he or she would be more comfortable under hospice care – or that a person they love will be on hospice care – there are steps you can take to get you through this difficult transition.


•If possible, make sure the whole family is on board and understands that hospice care is palliative (comfort) care. Hospice care is not meant to cure the incurable. To be eligible for hospice care, a doctor must already have stated that the person is terminally ill with a life expectancy of six months or less.


•Understand that hospice is simply care that helps a dying person live his or her last months as pain free as possible, and when possible, in a way that is meaningful to them. You and a hospice chaplain or other support person can explain to the ill person what hospice service provides. Hospice is not a "death sentence." A person's health can sometimes improve under hospice care. In that case, they go off the program.


•Hospice chaplains are trained in helping people through transitions. Let them guide you. Sometimes it's better for family members to take a backseat to hospice professionals when it comes to giving news of this sort, since the professionals have experience helping people understand this transition.


•Hospice staff members and volunteers don't dance around the term "death." They are there to deliver comfort care, and also help the person live their life until they die. Part of living the last months or weeks of life well is to understand and accept that one is dying. A dignified and meaningful death is the goal.


•Know that theory and reality can be different. Both of my parents wholeheartedly believed in hospice and the hospice mission. However, accepting and even championing an idea as opposed to having it apply personally can be quite different. Give the person who is going on a hospice care program time to grieve and accept the terminal diagnosis.


•Or – expect yourself to struggle with this concept, but note that your ill loved one may be relieved that he or she no longer needs to undergo unpleasant or painful treatments to no avail.


•People don't always respond in expected ways to the reality that they are dying. I've known people who've talked about "being with God" for years, yet when faced with their own impending death, they wanted to fight death all the way. That is their right. I've known others who seemed afraid of death throughout their lives only to experience a complete turnaround, facing impending death with faith and serenity.


•Every day won't be the same. Some days a person may accept or even seem to look forward to leaving a wrecked body behind, yet on another day, this same person could sink back into the grieving process. Be with them wherever they are.


•You and the hospice team are there to support the ill person in any way possible. Hospice care helps you share your loved one's last journey.


Hospice organizations understand that the life cycle includes death. The staff and volunteers believe in a dignified, pain free death for everyone, and they do all that is in their power to provide this kind of comfort care. Breaking the news that a loved one is on hospice care may be the hardest part of the experience.

After that concept is accepted, you can concentrate on supporting your loved one all the way through to the end. Work closely with the hospice team to understand every measure taken. Grieve with your loved one when grief is evident. Celebrate the person's memories with them. Respond to requests whenever possible, to increase mental, physical and emotional wellbeing for your loved one. Adjust your attitude to mesh with the hospice mission to help your loved one live well until he or she dies.

Wednesday, May 9, 2012

Effective pain relief for those with dementia

Health care providers, family members and others caring for those with dementia, here is some information on pain in people with dementia that you will find to be of great value.



People with dementia often have difficulty expressing their pain so those taking care of them can understand it. Also some drug pain relievers can bring about unwanted side effects.


So what is the alternative? Here are two alternative ways to reduce pain, TENS Units, and Muscle Stimulators . These items are cost effective and do not use drugs.


There is also a combination unit called the LG-TEC Dual Combo TENS Unit and Muscle Stimulator. You can visit LGMedSupply Online to get more information. In addition you can go to the online customer blog for more valuable information.


Tuesday, May 8, 2012

QuickMedical Announces Study Linking High Cholesterol Levels to Increased Risk for Developing Alzheimer's Disease or Vascular Dementia

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SeattlePI
According to QuickMedical, this new study should encourage more people to monitor their heart and brain health via cholesterol screening.


Issaquah, Wa (PRWEB) May 01, 2012
QuickMedical, a leading distributor of the CardioChek® cholesterol testing instrument for healthcare professionals, and the CardioChek® home cholesterol analyzer released a statement today hailing a new study by Kaiser Permanente. The study suggests that high cholesterol levels are a significant risk factor for developing dementia and Alzheimer's Disease later in life.


The results of the study were published in the journal of Dementia & Geriatric Cognitive Disorders. The research study tracked 9,844 men and women for four decades, starting when the participants were between 40 and 45 years of age.

After controlling for weight, hypertension and diabetes, the researchers discovered a significant link between borderline-high cholesterol and dementia.


The participants in the study, who had high cholesterol, or a value of 240mg/dl or more, had a 66 percent greater risk of developing Alzheimer's Disease later in life. People with borderline-high cholesterol, between 200 and 239, had a 25 percent spike in risk.


According to the American Heart Association, more than 106 million Americans reportedly have borderline-high cholesterol levels.


"With the availability of our CardioChek® cholesterol testing device for the healthcare professional and the CardioChek® analyzer for home use there is now a way for the public to know their cholesterol level number," said Robert Huffstodt, President and CEO of Polymer Technology Systems. "The continued emergence of research findings such as these strongly reinforces the rationale for including cholesterol screenings as an integral part of healthcare preventative maintenance; not only with regards to heart disease and diabetes, but now with the risk of dementia and Alzheimer's Disease.


The study concluded that people as young as 40 with borderline or high cholesterol levels are at increased risk for developing Alzheimer's disease or vascular dementia. Previous studies have linked heart and brain health, but this study is the first to examine the association between borderline cholesterol levels and dementia.







Sunday, May 6, 2012

A gift for a Mother with dementia



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Celebrate Mother's Day gift by choosing the right gift for someone with Alzheimer's disease or a related dementia This is certain to give him/her joyful times independently or with a loved one. Here are some tips on how to pick a perfect gift. You can give a gift anytime, but Mother's Day is coming soon which is a perfect opportunity to give that special someone a special gift.


Over 5.4 million Americans are living with dementia. Is one of them someone you know or a client of yours? Get him/her or anyone with Alzheimer's disease or another dementia, a gift that will keep on giving.


Of course, person appropriate offerings are the best. This means matching a gift to a person̢۪s interests and abilities, However, there are some presents that will make them smile no matter what.


One such gift is a book by Susan Berg called Adorable Photographs of Our Baby -- Meaningful, Mind-Stimulating Activities and More for the Memory Challenged, Their Loved Ones and Involved Professionals, This book features baby photographs that seniors with dementia love. This book shares a plethora of ideas and resources for you. Mothers especially love babies


Another gift dementia persons will fancy is a classic musical video or DVD especially a musical love story. A classic movie of this type is Rogers and Hammerstein̢۪s movie, Carousel (1945) or South Pacific (1949)


Any Roger's and Hammerstein movie is a good choice, However matching their interests and favorite actors and actresses should simplify the gift giving process. You can even discuss some of the movies to get a better feel for the one they might like the best.


A video sing along is great for persons who has Alzheimers disease or another dementia. Even if they were not music lovers in the past, music is extremely therapeutic for them. Often non-verbal folks with dementia will sing along to a song that is familiar to them. Russ Carlton has a series of videos that will enchant a person with dementia.


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Friday, May 4, 2012

Decline in Alzheimer's because of plaque and protein

Here is a great dementia resource for caregivers and healthcare professionals,


You will love the Amazon Kindle Fire


Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two


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UC San Diego Health Sciences News

Without p-tau protein present, impact of amyloid is “not significantly different from zero”


According to a new study, the neuron-killing pathology of Alzheimer’s disease (AD), which begins before clinical symptoms appear, requires the presence of both amyloid-beta (a-beta) plaque deposits and elevated levels of an altered protein called p-tau.


Without both, progressive clinical decline associated with AD in cognitively healthy older individuals is “not significantly different from zero,” reports a team of scientists in an issue of the Archives of Neurology.


“I think this is the biggest contribution of our work,” said Rahul S. Desikan, MD, PhD, research fellow and resident radiologist in the UC San Diego Department of Radiology and first author of the study. “A number of planned clinical trials – and the majority of Alzheimer’s studies – focus predominantly on a-beta. Our results highlight the importance of also looking at p-tau, particularly in trials investigating therapies to remove a-beta. Older, non-demented individuals who have elevated a-beta levels, but normal p-tau levels, maprogress to Alzheimer’s, while older individuals with elevated levels of both will likely develop the disease.”


The findings also underscore the importance of p-tau as a target for new approaches to treating patients with conditions ranging from mild cognitive impairment (MCI) to full-blown AD. An estimated 5.4 million Americans have AD. It’s believed that 10 to 20 percent of Americans age 65 and older have MCI, a risk factor for AD. Some current therapies appear to delay clinical AD onset, but the disease remains irreversible and incurable.


“It may be that a-beta initiates the Alzheimer’s cascade,” said Desikan. “But once started, the neurodegenerative mechanism may become independent of a-beta, with p-tau and other proteins playing a bigger role in the downstream degenerative cascade. If that’s the case, prevention with anti-a-beta compounds may prove efficacious against AD for older, non-demented individuals who have not yet developed tau pathology. But novel, tau-targeting therapies may help the millions of individuals who already suffer from mild cognitive impairment or Alzheimer’s disease.”


The new study involved evaluations of healthy, non-demented elderly individuals participating in the ongoing, multi-site Alzheimer’s Disease Neuroimaging Initiative, or ADNI. Launched in 2003, ADNI is a longitudinal effort to measure the progression of mild cognitive impairment and early-stage AD.

The researchers studied samples of cerebrospinal fluid (CSF) taken from ADNI participants



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