Sunday, April 29, 2018

Seven brain benefits of turmeric

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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



Salk Institute's J147 is a derivative of turmeric, a spice used in curry. Learn how it quickly reverses memory deficits and has a host of unexpected anti-aging effects in the lab. 




Salk Institute researchers have found that J147, which is an experimental drug candidate aimed at combating Alzheimer's disease, has a host of unexpected anti-aging effects in animals.

J147, Alzheimer's and Old Age

The Salk team expanded upon their previous development of the drug candidate they labeled J147. It is a derivative of the common spice, turmeric, and takes a different tack by targeting Alzheimer's major risk factor -- old age. In the new work, the team showed that the drug candidate worked well in a mouse model of aging not typically used in Alzheimer's research. When these mice were treated with J147, they had better memory and cognition, healthier blood vessels in the brain and other improved physiological features, as detailed in the journal Aging.

Fighting Alzheimer's By Fighting Aging

"Initially, the impetus was to test this drug in a novel animal model that was more similar to 99 percent of Alzheimer's cases," says Antonio Currais, the lead author and a member of Professor David Schubert's Cellular Neurobiology Laboratory at Salk. "We did not predict we'd see this sort of anti-aging effect, but J147 made old mice look like they were young, based upon a number of physiological parameters."

Alzheimer's disease is a progressive brain disorder, recently ranked as the third leading cause of death in the United States and affecting more than five million Americans. It is also the most common cause of dementia in older adults, according to the National Institutes of Health.

"While most drugs developed in the past 20 years target the amyloid plaque deposits in the brain (which are a hallmark of the disease), none have proven effective in the clinic," says Schubert, senior author of the study.

Expanding the Fight to More Common Dementias

Several years ago, Schubert and his colleagues began to approach the treatment of the disease from a new angle. Rather than target amyloid, the lab decided to zero in on the major risk factor for the disease--old age. Using cell-based screens against old age-associated brain toxicities, they synthesized J147.

Previously, the team found that J147 could prevent and even reverse memory loss and Alzheimer's pathology in mice that have a version of the inherited form of Alzheimer's, the most commonly used mouse model. However, this form of the disease comprises only about 1 percent of Alzheimer's cases. For everyone else, old age is the primary risk factor, says Schubert. The team wanted to explore the effects of the drug candidate on a breed of mice that age rapidly and experience a version of dementia that more closely resembles the age-related human disorder.

Young Mice, Old Mice and J147-fed Mice

In this latest work, the researchers used a comprehensive set of assays to measure the expression of all genes in the brain, as well as over 500 small molecules involved with metabolism in the brains and blood of three groups of the rapidly aging mice. The three groups of rapidly aging mice included one set that was young, one set that was old and one set that was old but fed J147 as they aged.

7 Benefits

The old mice fed J147 saw the following benefits:
  1. They performed better on memory and other tests for cognition
  2. They displayed more robust motor movements.
  3. They had fewer pathological signs of Alzheimer's in their brains.
  4. J147 prevented the leakage of blood from the microvessels in the brains of old mice. "Damaged blood vessels are a common feature of aging in general, and in Alzheimer's, it is frequently much worse," says Currais.

    Importantly, because of the large amount of data collected on the three groups of mice, it was possible to demonstrate that many aspects of gene expression and metabolism in the old mice fed J147 were very similar to those of the young animals. These included:
  5. markers for increased energy metabolism,
  6. reduced brain inflammation and
  7. reduced levels of oxidized fatty acids in the brain.

Human Clinical Trials

Currais and Schubert note that while these studies represent a new and exciting approach to Alzheimer's drug discovery and animal testing in the context of aging, the only way to demonstrate the clinical relevance of the work is to move J147 into human clinical trials for Alzheimer's disease.

"If proven safe and effective for Alzheimer's, the apparent anti-aging effect of J147 would be a welcome benefit," adds Schubert. The team aims to begin human trials next year.


Friday, April 27, 2018

Does fish oil improve dementia

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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

ADNI (The Alzheimer's Disease Neuroimaging Initiative) is one of the world's largest Alzheimer's research projects. ADNI researchers examined how fish oil supplements relates to improvements in cognitive decline and brain atrophy. What they found is worth knowing. 




PROVIDENCE, R.I. –Rhode Island Hospital researchers have completed a study that found regular use of fish oil supplements (FOS) was associated with a significant reduction in cognitive decline and brain atrophy in older adults. The study examined the relationship between FOS use during the Alzheimer's Disease Neuroimaging Initiative (ADNI) and indicators of cognitive decline. The findings are published in the journal, Alzheimer's & Dementia.

"At least one person is diagnosed every minute with Alzheimer's disease (AD) and despite best efforts, we have not yet found a cure for this pervasive and debilitating disease," said principal investigator Lori Daiello, PharmD, of the Alzheimer's Disease and Memory Disorders Center at Rhode Island Hospital. "The field is currently engaged in numerous studies to find better treatments for people suffering with AD; however, researching ways to prevent AD or slow cognitive decline in normal aging is of utmost importance."

In this retrospective study, older adults involved in the ADNI study were assessed with neuropsychological tests and brain magnetic resonance imaging (MRI) every six months. The group included 229 older adults who were cognitively normal; 397 who were diagnosed with mild cognitive impairment; and 193 with AD.

The study found that fish oil supplement use during the study was associated with significantly lower rates of cognitive decline as measured by the Alzheimer's Disease Assessment Scale (ADAS-cog), and the Mini Mental State Exam (MMSE), but this benefit was observed only for the group of participants without dementia at the time of enrollment.

"Additionally, serial brain imaging conducted during this study showed that the participants with normal cognition who reported taking fish oil supplements demonstrated less brain shrinkage in key neurological areas, compared to those who did not use the supplements," Daiello said. "Also, the positive findings on cognitive testing and brain MRI were only observed in persons who did not carry the best-studied genetic risk factor for AD, APOE-4. More research is needed, but these findings are promising and highlight the need for future studies to expand the current knowledge of the effects of FOS use on cognitive aging and AD."


his research was funded by from the Agency for HealthCare Research and Quality (AHRQ) (K08 HS017735); National Institute on Alcohol Abuse and Alcoholism (NIAAA) (R00AA020235, P01AA019072, and R01NS080655); National Cancer Institute (R03 CA153942, R01 CA155381); National Institute of Nursing Research (R01 NR011295); National Heart, Lung and Blood Institute (R01HL109116, R01 CA159954, 5T32HL076134, R01 HL064342); National Center for Complementary and Alternative Medicine (R01AT006948); National Institute on Drug Abuse (R01 DA021729, R34 DA031057); National Institute of Diabetes and Digestive Kidney Disorders (R18 DK075371); National Institutes of Health (R01 HL089311, U01 CA1503878; R34 DA031057-02, P01 AA019072, R01 NS036524, R01 HL084178, R01 DA020725, R56 DK075119, and R01 MH074368); and support from Pfizer; Janssen; Baxter, Eli Lilly and Avid pharmaceutical companies. Daiello's principal affiliation is Rhode Island Hospital, and she also holds academic appointments in the department of neurology (research) at The Warren Alpert Medical School of Brown University and Health Services, Policy & Practice in the Brown University School of Public Health. Other current and former Lifespan researchers involved in the study are Brian Ott, M.D (Rhode Island Hospital; Shira Dunsiger, Ph.D, of The Miriam Hospital, Assawin Gongvatana, Ph.D (University of California San Diego), and Ronald A. Cohen, Ph.D., (University of Florida).

About Rhode Island Hospital

Founded in 1863, Rhode Island Hospital in Providence, R.I., is a private, not-for-profit hospital and is the principal teaching hospital of The Warren Alpert Medical School of Brown University. A major trauma center for southeastern New England, the hospital is dedicated to being on the cutting edge of medicine and research. Last year, Rhode Island Hospital received more than $55 million in external research funding. It is also home to Hasbro Children's Hospital, the state's only facility dedicated to pediatric care. For more information on Rhode Island Hospital, visit http://www.rhodeislandhospital.org, follow us on Twitter @RIHospital or like us on Facebook http://www.facebook.com/rhodeislandhospitalpage.

Wednesday, April 25, 2018

Better lighting better dementia life

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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

 The Alzheimer’s Disease Education and Referral (ADEAR) Center, a service of the National Institute on Aging, part of the National Institutes of Health




For more caregiving tips and other resources:

  1. Visit http://www.nia.nih.gov/alzheimers/topics/caregiving
  2. Call the ADEAR Center toll-free:
    1-800-438-4380
SOURCE: The Alzheimer’s Disease Education and Referral (ADEAR) Center, a service of the National Institute on Aging, part of the National Institutes of Health

Monday, April 23, 2018

Three new drugs for Alzheimer's

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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



n the lab, fujimycin slowed Alzheimer's. (Fujimycin is an organ-transplant drug also called FK506 or Tacrolimus.) In past studies, similar drugs, like rapamycin and ciclosporin, also lowered rates of Alzheimer's. Learn how these immunosuppressants show great promise in the fight against Alzheimer's. 




Studies in mice provide new clues about how a class of anti-rejection drugs used after organ transplants may also slow the progression of early-stage Alzheimer's disease. These drugs are known to be immunosuppressants.

Fujimycin (FK506) Rescued Synapses from Alzheimer's

FK506 is the lab name for fujimycin, also known as Tacrolimus. It is part of a class of drugs that are immunosuppressants that have been associated with less Alzheimer's. Other qualified successes
 were previously seen in rapamycin and ciclosporin



At UT Southwestern, Dr. James Malter explained that nerve cells initially lose dendritic spines, tiny branchlike extensions at the ends of neurons that receive information across synapses from nearby cells. Synapses -- the junctions where communication between neurons occurs -- are also lost. The area of the brain that is most affected governs higher-order functions such as language, spatial reasoning, conscious thinking, sight, hearing, and other senses.

"We found that beta-amyloid, which is overproduced in the brains of most people with Alzheimer's, turns on a protein called calcineurin. Activated calcineurin then causes the inhibition of a second protein called Pin1, leading to loss of dendritic spines and synapses," said Dr. Malter, who holds The Senator Betty and Dr. Andy Andujar Distinguished Chairmanship of Pathology.

In experiments in neurons and in genetically engineered mice unable to produce Pin1, the researchers were able to duplicate the loss of dendritic spines and synapses even in the absence of exposure to beta-amyloid, demonstrating a critical role for Pin1 in this process.

Fujimycin FK506 Rescues Synapses

"In additional experiments, we showed that synapses could be rescued if the neurons received extra Pin1 or were exposed to FK506 -- a drug that blocks calcineurin and is currently approved by the Food and Drug Administration [FDA] for the prevention of solid organ transplant rejection. The oldest drug in this class, cyclosporin, has been used since 1983," Dr. Malter said.

Intriguingly, a recent study from UT Medical Branch at Galveston showed that patients who receive FK506 for long-term immunosuppression following transplant, developed Alzheimer's less frequently than expected.

"As an FDA-approved drug, we propose that FK506 be evaluated through clinical trials as a treatment for early-stage Alzheimer's disease," Dr. Malter said. "Anti-rejection drugs given to organ transplant recipients work by suppressing the immune system and, as a result, can increase the risk of infection. Our experiments suggest that lower doses of FK506 than are needed to block transplant rejection may be able to protect neurons from beta-amyloid without significant immunosuppression."

Cyclosporin Blocks Amyloid Beta Plaque

At Columbia University Medical Center, another potential drug, cyclosporin, is already used in organ transplant and autoimmune patients. Cyclosporin suppresses the immune system, but it also blocks amyloid beta (Aβ) peptides-induced mitochondrial injury. (See previous studies Du et al. Nature Medicine, 2008).

Cyclosporin, however, has too many toxic side effects for long term use in other patients. Dr. ShiDu Yan is currently trying to alter the chemical structure of the drug to reduce its toxicity and to improve its ability to cross the blood brain barrier but preserve its protective effect on Aβ-mediated toxicity.

Most Alzheimer's researchers initially believed that Aβ peptides caused the disease after aggregating together in large, extracellular plaques, a defining feature of Alzheimer's-affected brains. But Dr.Yan's findings, along with those of many other scientists, now point to an earlier role for Aβ peptides inside the brain's neurons.

The mitochondria are damaged, the researchers found, when (Aβ) peptides breach the mitochondria's walls and accumulate on the inside. Even low concentrations of Aβ peptides, equivalent to the levels found in cells years before symptoms appear, impair the mitochondria, particularly mitochondria that supply power to the neuron's synapses.

When filled with Aβ peptides, these synaptic mitochondria were unable to travel down the neurons' long axons to reach, and fuel, the synapse. And the mitochondria that did make the journey failed to provide adequate energy to operate the synapses. Without operating synapses, neurons are unable to function.

"Since cyclosporin is already FDA approved for use in organ transplant and autoimmune patients, this research has the potential to lead to more rapid clinical trials and progress quickly," said Dr. Yan.

Rapamycin Study

At the UT Health Science Center San Antonio, mice that model Alzheimer's were fed food containing rapamycin for 10 weeks. At the start of treatment the mice were 6 months old, roughly the age of young adults. They already exhibited learning and memory deficits and brain lesions.

At the end of the 10 weeks, the mice were tested in a Morris water maze to assess learning and memory in rodents. Then the brains of the mice were analyzed to determine the effects of rapamycin on the lesions that indicate Alzheimer's.

Senior Author Dr. Salvatore Oddo said, "While it remains to be determined whether our results obtained in mice could be translated in people, we are very excited as these findings may lead to a new therapeutic intervention to treat Alzheimer's."

REFERENCES:
MORE INFORMATION:
  • UTSW co-authors include Dr. Ege Kavalali, Professor of Neuroscience and Physiology; Dr. Ilya Bezprozvanny, Professor of Physiology; and Dr. Jie Hu, a research scientist in Pathology. Dr. Bezprozvanny holds the Carl J. and Hortense M. Thomsen Chair in Alzheimer's Disease Research. Dr. Kavalali, an Effie Marie Cain Scholar in Medical Research, holds the Rosewood Corporation Chair in Biomedical Science.
  • The study was supported by the Senator Betty and Dr. Andy Andujar Endowment and by the National Institutes of Health.
SOURCE:

Saturday, April 21, 2018

Beware of over the counter drugs

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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



See how Benadryl and dozens of anticholinergic drugs show a strong link to Alzheimer's and dementia risk. Learn about alternatives. Take advantage of "The Anticholinergic Pocket Reference Card" for the elderly and people with dementia.




A large study links a significantly increased risk for developing dementia, including Alzheimer's disease, to taking commonly used medications with anticholinergic effects at higher doses or for a longer time. Many older people take these medications, which include nonprescription diphenhydramine (Benadryl). 

Continued below video...


JAMA Internal Medicine published the report, called "Cumulative Use of Strong Anticholinergic Medications and Incident Dementia."

If You Have Dementia, Take Additional Care with Common Anticholinergic Drugs
Benadryl
Acetylcholine activates the brain cells we use for memory and thinking. Alzheimer's drugs boost acetylcholine. Common anti-cholinergic drugs lower acetylecholine, which could mean trouble for people with dementia. Learn which drugs to avoid and what to look out for.
The study used more rigorous methods, longer follow-up (more than seven years), and better assessment of medication use via pharmacy records (including substantial nonprescription use) to confirm this previously reported link.

First Study

It is the first study to show a dose response: linking more risk for developing dementia to higher use of anticholinergic medications. And it is also the first to suggest that dementia risk linked to anticholinergic medications may persist -- and may not be reversible even years after people stop taking these drugs.
"Older adults should be aware that many medications -- including some available without a prescription, such as over-the-counter sleep aids -- have strong anticholinergic effects," said Shelly Gray, PharmD, MS, the first author of the report, which tracks nearly 3,500 Group Health seniors participating in the long-running Adult Changes in Thought (ACT), a joint Group Health-University of Washington (UW) study funded by the National Institute on Aging. "And they should tell their health care providers about all their over-the-counter use," she added.

"But of course, no one should stop taking any therapy without consulting their health care provider," said Dr. Gray, who is a professor, the vice chair of curriculum and instruction, and director of the geriatric pharmacy program at the UW School of Pharmacy. "Health care providers should regularly review their older patients' drug regimens -- including over-the-counter medications -- to look for chances to use fewer anticholinergic medications at lower doses." 
For instance, the most commonly used medications in the study were

  • Tricyclic antidepressants like doxepin (Sinequan)
  • First-generation antihistamines like chlorpheniramine (Chlor-Trimeton)
  • Antimuscarinics for bladder control like oxybutynin (Ditropan)
The study estimated that people taking at least 10 mg/day of doxepin, 4 mg/day of chlorpheniramine, or 5 mg/day of oxybutynin for more than three years would be at greater risk for developing dementia. Dr. Gray said substitutes are available for the first two:
  • A selective serotonin re-uptake inhibitor (SSRI) like citalopram (Celexa) or fluoxitene (Prozac) for depression
  • A second-generation antihistamine like loratadine (Claritin) for allergies
It's harder to find alternative medications for urinary incontinence, but some behavioral changes can reduce this problem.

"If providers need to prescribe a medication with anticholinergic effects because it is the best therapy for their patient," Dr. Gray said, "they should use the lowest effective dose, monitor the therapy regularly to ensure it's working, and stop the therapy if it's ineffective." Anticholinergic effects happen because some medications block the neurotransmitter called acetylcholine in the brain and body, she explained. That can cause many side effects, including drowsiness, constipation, retaining urine, and dry mouth and eyes.

"With detailed information on thousands of patients for many years, the ACT study is a living laboratory for exploring risk factors for conditions like dementia," said Dr. Gray's coauthor Eric B. Larson, MD, MPH. "This latest study is a prime example of that work and has important implications for people taking medications -- and for those prescribing medications for older patients." Dr. Larson is the ACT principal investigator, vice president for research at Group Health, and executive director of Group Health Research Institute (GHRI). He is also a clinical professor of medicine at the UW School of Medicine and of health services at the UW School of Public Health.

Some ACT participants agree to have their brains autopsied after they die. That will make it possible to follow up this research by examining whether participants who took anticholinergic medications have more Alzheimer's-related pathology in their brains compared to nonusers

Friday, April 20, 2018

Tax savings ideas for seniors

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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

Digital Journal

For a country with little in the way o state support or socialized healthcare, the elderly in the U.S. who are of low income face a number of challenges. These challenges include finding the money to pay for a nursing home, or an assisted living facility or another form of care. However, there are solutions of the U.S. population in terms of tax deductions that can be taken advantage of. These deductions can provide extra money to help with long-term care expenses, according Chris Orestis, who is the Executive Vice President of GWG Life.
Orestis has recently published the book Help on the Way, which provides guidance about long term care benefit plans and information about Medicare and Medicaid. The book also provides guidance on the various forms of senior care and the legal rights of owning life insurance. Orestis has also written the text A Survival Guide to AgingThis second book focuses on issues such as long term care planning, improved longevity through exercise, eating, and healthy lifestyles, legal and political issues, events in the news, and interesting stories that can help shine a light on making the most out of peoples’ Senior Living years.
Orestis has provided Digital Journal readers with three tips for U.S. citizens thinking about their future care plans. These are:
Costs of senior living and long-term care.
Orestis writes "If you’re diagnosed as chronically ill, some long-term care expenses can be tax deductible." These expenses need to be more than 7.5 percent of a person's adjusted gross income. Orestis defines“chronically ill” as: “You must be diagnosed and under a certified care plan issued by a doctor or nurse that addresses your inability to perform two or more activities of daily living."
He also adds: "Or you need to be suffering from cognitive impairments....Family members may also be entitled to tax deductions if they are financially contributing to the costs of care for a loved one and qualify as a dependent."
Long-term care insurance premiums
Here owners of long-term care insurance policies can take tax deductions on premiums they pay for qualified plans – as well as other reimbursed medical expenses such as Medicare premiums – as long as the premiums are greater than 7.5 percent of adjusted gross income, according to Orestis.
Estate tax changes and life insurance
It is notable that many U.S. based large life insurance policies were purchased over the years as a wealth and legacy-preservation strategy to offset the impact of estate taxes. Orestis states that: "Prior to tax reform, the first $5,490,000 of income was exempt from the estate tax. Now that has been nearly doubled to $10 million. “That means policies currently in force to protect estates valued below the new level are no longer necessary."
He expands: "This presents a chance for the policy owner to sell the policy and recoup some or all of their premium payments under more advantageous tax conditions.”
In offering these tips, Chris Orestis aims to help elderly people in the U.S. understand the tax rules and how they apply to their personal situation, and to use this to help with care solutions.

Read more: http://www.digitaljournal.com/life/health/three-tax-savings-ideas-to-help-seniors/article/519963#ixzz5DEND71gp

Monday, April 9, 2018

Lower salt intake to boost brain health

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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

NINDS (NS089323, NS095441), the American Heart Association, and the Fondation Leducq, Paris. 

A HIGH-SALT-DIET impaired blood flow in the brain, causing dementia-like symptoms in the lab. Can lowering the ingestion of added-salt improve brain-health? 




We are often warned of the dangers of 
levels of salt in our diet, yet the risks of salt consumption and the effects of salt on the body, including the brain, are not entirely clear. In a new mouse study, scientists link changes in the gut caused by a high-salt diet to impaired blood flow in the brain. This reduced blood flow can eventually lead to impaired cognition that could be reversed by changing back to a normal diet. The study, published in Nature Neuroscience, also provides molecular clues for treating these problems. 




“For years researchers have wondered how a high-salt diet harms the brain,” said Jim Koenig, Ph.D., program director at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, which supported the study. “This mouse study provides a detailed cellular and molecular diagram for how the problems start in the gut and opens unexpected paths towards new treatments.”

In this study, mice were fed a high-salt diet (HSD) containing 16 times the amount of sodium chloride typically found in their food. After eight weeks, their brains showed a 20 to 30 percent reduction in blood flow compared to mice that ate normal food. This drop in blood flow was accompanied by the appearance of dementia-like symptoms, including defects in the ability of HSD mice to recognize objects, navigate a maze, and properly build a nest. When the mice were returned to a normal diet, both blood flow and cognition improved, suggesting that the negative effects of excessive salt consumption could be reversible.

“The brain is extremely dependent on getting the right amount of blood at the right time. If blood flow isn’t matched to what the brain needs, things go wrong,” said Costantino Iadecola, M.D., director and chair of the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine in New York City and senior author of this study.

To study further how salt affects blood flow in the brain, blood vessels were taken from the brains of mice fed a high-salt diet and grown in a dish. Normally, these vessels tighten (constrict) to reduce blood flow or relax (dilate) to increase flow. However, those taken from HSD mice did not dilate properly when stimulated to do so. A closer look revealed a reduction in the function of the enzyme eNOS that is responsible for producing nitric oxide (NO), a potent signal for blood vessels to dilate.

When the amino acid L-arginine, which can increase eNOS activity and NO production, was added to the dishes containing blood vessels from HSD mice, the cells responded normally. When L-arginine was injected into HSD mice directly, the defects in cognition were also rescued.

“These findings together show that a high-salt diet affects the activity of the eNOS enzyme, which in turn leads to problems with blood flow and cognition,” said Dr. Iadecola, who is on the strategic advisory board and receives a consulting fee from Broadview Ventures Inc. Broadview Ventures Inc. was created by the board of the Foundation Leducq Trust, the supporting trust of Foundation Leducq, “But the question still remained how the ingestion of salt could lead to these effects in the brain.”

One clue came from evidence showing that eating high levels of salt changes the immune system of the gut, a finding that was first reported by scientists studying salt’s effects in a model of multiple sclerosis. Specifically, a high-salt diet increased the appearance of TH17 immune cells. These TH17 cells secrete a molecule, IL-17, that can have toxic effects on blood vessels. Because the researchers did not observe any TH17 cells in the brains of HSD mice, they concluded that it must be IL-17, moving throughout the circulatory system, that was acting directly on the brain’s blood vessels.

The combined results of three additional experiments helped to confirm this hypothesis. First, HSD produced no effects in the brains of mice that lacked the gene for IL-17. Second, the effects of HSD could be reversed by treating mice with an antibody that binds up IL-17 and prevents it from affecting blood vessels. Third, effects similar to those produced by HSD were seen in normal mice that were injected directly with IL-17. Together, these findings suggest that it is IL-17, released from cells in the gut in response to a high-salt diet, that acts on the blood vessels in the brain to affect blood flow.

In humans, high levels of salt in the diet has long been associated with high blood pressure, and increasing evidence has linked blood pressure and brain health. However, the blood pressure of HSD mice was not affected, suggesting a very specific and independent mechanism for the changes seen here.

“This study adds to our growing understanding of how the gut can modulate brain function,” said Dr. Koenig. “From a public health perspective, the fact that these effects can be reversed by halting the ingestion of salt is very important and could help us improve health in areas where many people eat a high-salt diet.”

In future experiments, Dr. Iadecola and his colleagues plan to further investigate further how decreased NO production and reduced blood flow leads to changes in cognition.

SOURCE:
  • This work was supported by the NINDS (NS089323, NS095441), the American Heart Association, and the Fondation Leducq, Paris.

    The NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

    About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

    NIH…Turning Discovery Into Health®

    Reference Faraco et al. Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response. Nature Neuroscience. January 15, 2018. doi: 10.1038/s41593-017-0059-z

Saturday, April 7, 2018

Use the right words when communicating with those who have dementia

Caregivers, and healthcare professionals,here is some great information

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

Your residents 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

Follow alzheimersideas on twitter

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

University of York

BETTER COMMUNICATION: 

Which words are easier and harder for people with dementia? When finding the right word or comprehending a complex phrase becomes difficult, helpful research gives clarity on which word types work best. 




Scientists say they have a better understanding of why people with Alzheimer's struggle to recognize and understand words - and their research has the potential to be developed into a test which could help clinicians make an early diagnosis.

Word Complaints

In the early stages, the two most common complaints from people with Alzheimer's disease are difficulty remembering events and understanding and producing words.

Academics from the Universities of York and Oviedo, Spain, wanted to look at whether a patient's ability to recognize words is impaired in the early stages of the disease, and if it is, what properties of words make them easier or harder for a patient to recognize.

The research, which was done in northern Spain with colleagues at the Hospital Cabueñes in Gijón, was published in theJournal of Neuropsychology.

Word Diagnosis

A test of word recognition based on the findings could contribute to diagnosis, Professor Andrew Ellis, from the Department of Psychology at York, said.

He added: "The biggest potential impact is in diagnosis. It might be a useful addition to the armory of clinicians trying to do diagnosis.

"Alzheimer's disease isn't easy to diagnose in the early stages. There are other forms of dementia that are relatively common and it can be hard to distinguish between them in the early stages. A word recognition test based on these findings could contribute to diagnosis, but more work would need to be done."

Real Words versus Invented Words

As part of the study, participants were shown real words on a computer screen mixed with invented words. On each trial of the experiment, there was one real word on the screen and three non-words. The participant's task was simply to point to the real word on the screen.

Researchers chose the task primarily because it assesses whether words look familiar or not and does not require the patients to explain the meanings of words, something they struggle to do.

They conducted the study in Spanish but an example in English would be to point to the word EAGLE when it appears on the screen with SLINT, OMPUL and CROOM. The researchers chose words which they expected healthy older people to be able to recognize.

Forty people with mild or moderate Alzheimer's disease aged 66 to 91 years took part in the study, and 25 healthy controls matched to the patients on age, gender and years of education. The healthy controls picked out the real words with little difficulty, from which the scientists infer that the patients would also have known these words before the onset of their dementia.

In contrast, the patients with Alzheimer's disease missed about one in five of the real words. When the researchers looked at which properties of the words made them easier or harder for patients to recognise, they found that:
  1. COMMON WORDS: Patients recognised common words better than less common words
  2. ABSTRACT WORDS: Patients understood words with concrete meanings better than words with abstract meanings
  3. CHILDHOOD WORDS: Patients grasped words learned early in life better than words learned in later childhood or adulthood.
  4. LONG WORDS: The length of the words did not affect performance.

Ability to Use Words

Professor Ellis added: "A lot of work has been done with Alzheimer patients using the task of naming pictures of objects.

"In this study we wanted to look instead at whether their ability to recognise words is impaired in the early stages of the disease. If word recognition is impaired, we wanted to know what properties of words make them easier or harder for Alzheimer patients to recognise.

"We speculate that the damage responsible for the problems in word recognition and production that we and other researchers have identified, stem particularly from loss of cells in an area at the front of the left temporal lobe that is crucially involved in processing the meanings of concepts and words.

"The study is fundamental rather than applied research. Its purpose is to teach us more about how Alzheimer's disease affects the ability to use words, but it also has the potential to inform the clinical assessment of dementia."
Blog Flux Directory
alzheimersideas - whereIstand.com

Fitness is important in dementia prevention. Click below for more info