Showing posts with label dementia risk. Show all posts

Tuesday, July 23, 2019

How to lower dementia risk with hearing loss treatment

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]
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hear.com — simply good hearing

PREVENTION & THERAPY INFOMERCIAL:

Research shows that for every 10 decibels of hearing loss, the risk of developing dementia increases. Learn how the right hearing aids can lower your risk.

Hearing Loss & Dementia

Researchers from John Hopkins recently completed an 18-year study showing participants who experienced hearing loss had an increased risk of developing dementia. A person’s risk of developing dementia increased with the severity of hearing loss. In another study, Gallacher et al concluded that for every 10 decibels of hearing loss, the risk of developing dementia increased.

How does hearing loss impair the brain? When the ears stop hearing certain sounds and frequencies, the brain turns off the areas needed to process those sounds. The brain also begins to shrink. MRIs show that adults with untreated hearing loss lose about a cubic centimeter of brain tissue per year.

Hearing Aids May Lower the Risk of Dementia

Hearing aids receive sounds from your environment and only amplify the sounds your ears had stopped perceiving. This technology enables the brain to recognize and process those frequencies again. Therefore, the brain continues working in those areas! By keeping your brain engaged, brain shrinkage occurs more slowly and the risk for developing dementia may be lowered.

Hearing aids also help people maintain physical, emotional, and cognitive health by giving them the chance to participate in conversations and social activities. Surveys conducted in Europe revealed hearing aid users are less tired at the end of the day and have more restful sleeps. Hearing aids users are also less depressed. In conclusion, hearing aids provide many benefits, from keeping you happy to keeping your brain healthy.

To learn more about hearing aids and how to start wearing them, request a free consultation from hear.com. Knowledgeable experts will connect you with the top hearing specialists in your area and provide you with the most effective hearing aids available.

Start your consultation now »

SOURCE:

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Friday, June 8, 2018

Decrease dementia risk with normal blood sugars

A joint Group Health-University of Washington (UW) study in the New England Journal of Medicine has found that higher blood sugar levels are associated with higher dementia risk, even among people who do not have diabetes. (Continued below video.)

Continued below video...

Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, in this report about more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study.

There was No Level Where Risk Leveled Off

For example, in people without diabetes, risk for dementia was 18 percent higher for people with an average glucose level of 115 milligrams per deciliter compared to those with an average glucose level of 100 mg/dl. And in people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40 percent higher for people with an average glucose level of 190 mg/dl compared to those with an average glucose level of 160 mg/dl.

"The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes," said first author Paul K. Crane, MD, MPH, an associate professor of medicine at the UW School of Medicine, adjunct associate professor of health services at the UW School of Public Health, and affiliate investigator at Group Health Research Institute. "There was no threshold value for lower glucose values where risk leveled off."

Very Rich Data

"One major strength of this research is that it is based on the ACT study, a longitudinal cohort study, where we follow people for many years as they lead their lives," said senior author Eric B. Larson, MD, MPH, a senior investigator at Group Health Research Institute who also has appointments at the UW Schools of Medicine and Public Health. "We combine information from people's research visits every other year with data from their visits to Group Health providers whenever they receive care. And this gave us an average of 17 blood sugar measurements per person: very rich data."

These measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c). Blood sugar levels rise and fall in peaks and valleys throughout each day, but glycated hemoglobin doesn't vary as much over short intervals.

Combining glucose and glycated hemoglobin measures into a composite measure required special statistical techniques, which Drs. Crane and Larson's co-authors Rod Walker, MS, a biostatistician, and Rebecca Hubbard, PhD, an associate investigator, both from Group Health Research Institute, had developed. (Dr. Hubbard is also an affiliate assistant professor of biostatistics at the UW School of Public Health.) These sophisticated statistical models required specialized data on the relationships between glycated hemoglobin and glucose levels, and they used data generated by co-author David M. Nathan, MD, a professor of medicine at Harvard Medical School and director of the Diabetes Center at Massachusetts General Hospital.

Saturday, February 3, 2018

Can adding salt to food increase Alzheimer's risk

This work was supported by the 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 high 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.

Monday, June 19, 2017

Western Diet Increases Alzheimer’s Pathology in Genetically Predisposed Mice

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

Neuroscience News

summary: Diet and lifestyle changes could lower the risk of developing Alzheimer’s disease for those who are genetically predisposed, a new study suggests.

Source: SfN.

Obese mice with a particular version of a gene strongly associated with Alzheimer’s disease (AD) in humans show increased Alzheimer’s pathology, according to new research published in eNeuro. The study suggests lifestyle changes could reduce the likelihood of developing AD in individuals with this genetic predisposition.

Individuals who inherit the gene APOE4 — approximately 12 percent of the U.S. population — have an increased risk of late-onset AD, but not all carriers develop the disease. Although the role of APOE4 in AD is not known, environmental factors that also increase risk of dementia, such as obesity, may contribute to development of AD.

Christian Pike and Alexandra Moser investigated the interaction between APOE4 and obesity in a mouse model of AD, in which some male mice carry the human version of APOE4 and others carry the more common human version APOE3. The authors found that APOE4-carrying mice fed a Western-like diet high in saturated fat and sugars for 12 weeks had increased deposits of β-amyloid protein as well a greater number of glial cells, characteristic of AD. These changes were not observed in mice carrying APOE3, which could mean that carriers of APOE4 are more susceptible to the effects of obesity on AD.

The authors found that APOE4-carrying mice fed a Western-like diet high in saturated fat and sugars for 12 weeks had increased deposits of β-amyloid protein as well a greater number of glial cells, characteristic of AD. NeuroscienceNews.com image is for illustrative purposes only.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: SfN
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in eNeuro.

Thursday, August 30, 2012

Potassium, calcium, magnesium intakes linked to reduced risk of dementia

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

FoodConsumer

By David Liu, PHD

(foodconsumer.org) -- A new study in Journal of American Geriatrics Society suggests that taking potassium, calcium and magnesium supplements or eating foods high in these minerals may help prevent some forms of dementia, but not Alzheimer's disease.

The study led by M. Ozawa of Kyushu University om Fukuoka Japan and colleagues showed that all-cause dementia was 48 percent, 36 percent, and 37 percent less likely among people with highest intakes of potassium, calcium, and magnesium, respectively, compared to those who had low levels.

A total of 1081 community dwelling Japanese people without dementia aged 60 or older participated in the study in which 303 participants were found to have all-cause dementia including 98 vascular dementia and 166 Alzheimer's disease during a 17-year follow-up.

Participants who had highest intakes of potassium, calcium and magnesium were 80 percent, 77 percent and 74 percent less likely to develop vascular dementia, respectively, compared to those who had lowest intakes.

But these minerals were not associated with risk of Alzheimer's disease.

The researchers concluded that high dietary intakes of potassium,calcium, and magnesium reduce risk of all cause dementia, particularly vascular dementia in the general Japanese population.

Alzheimer's disease is a major form of dementia affecting an estimated 5 million Americans. There is no cure for Alzheimer's but research suggests that the disease is preventable.

Monday, June 25, 2012

Does the way you walk affect your risk of getting dementia

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

CTV.ca

As the American Academy of Neurology points out, dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems, such as agitation, delusions, and hallucinations.

While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions -- such as memory and language skills -- are significantly impaired without loss of consciousness. Although it is common in very elderly individuals, dementia is not a normal part of the aging process.

Research in this week’s issue of Neurology, shows that changes in walking speed in late life may signal the early stages of dementia known as mild cognitive impairment (MCI).

The study used a new technique that included installing infrared sensors in the ceilings of homes, a system designed to detect walking movement in hallways to get a better idea of how even subtle changes in walking speed may correlate with the development of MCI.

The study involved 93 people age 70 or older who lived alone. Of those, 54 participants had no cognitive impairment, 31 had non-memory related MCI and eight had memory-related MCI. Participants were given memory and thinking tests and had their walking speed monitored at their homes unobtrusively over a three-year period. Participants were placed in groups of slow, moderate or fast based on their average weekly walking speed and how much their walking speed fluctuated at home.

The study found that people with non-memory related MCI were nine times more likely to be slow walkers than moderate or fast walkers and the amount of the fluctuation in walking speed was also associated with MCI.

As the authors point out, if we can detect dementia at its earliest phases, then we can work to maintain people's independence, provide treatments and ultimately develop ways to prevent the disease from developing.

Presented today at the International Conference on Social Identity and Health is a study on attitude towards our age. The study looked at the how our attitude has a massive impact on the likelihood of being diagnosed with dementia. Their research shows that when seniors see themselves as 'older' their performance on a standard dementia screening test declines dramatically; making them five times more likely to meet the criteria for dementia.

The research involved 68 people aged between 60 and 70 years, who were primed to either feel older or younger than others taking part in the study. Those in the 'older' group were told the participants ranged in age from 40 to 70, encouraging them to think of themselves as being at the upper end of the age spectrum, while those in the 'younger' group were told that participants ages ranged from 60 to 90 years, encouraging them to think of themselves at the lower end of the age spectrum. All participants were then given one of two articles to read, which either focused on the effects of age on memory loss or on the impact of ageing on general cognitive ability.

The participants then completed a series of standard clinical tests; 70 per cent of people, who were encouraged to see themselves as older and to believe that aging was associated with a general decline in ability, met the criterion for dementia. This was compared to an average of 14 per cent in the other groups.

The research shows that the effect of age perceptions on performance can be dramatic, and that seeing oneself as 'older' significantly increases a person's risk of being diagnosed with dementia on such tests. It highlights the importance of taking a person's attitude towards their age into account when assessing for dementia.

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.

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, September 25, 2011

Calcified Plaque in Arteries May Pose Stroke, Dementia Risk

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American Heart Association
Calcified Plaque in Arteries May Pose Stroke, Dementia Risk
American Heart Association Rapid Access Journal Report
Study Highlights:

Calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke.
The results may help understand how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.

Greater calcium build-up in blood vessels outside the brain may be associated with brain changes linked to future risk of dementia and stroke, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association.

"The relationship between calcium in atherosclerotic plaque and brain changes exists on top of the effect of classic cardiovascular risk factors such as high blood pressure, smoking and diabetes," said Meike W. Vernooij, M.D., Ph.D., senior study author and assistant professor of epidemiology and radiology at the Erasmus Medical Center in Rotterdam, the Netherlands.

Furthermore, the amount of hardened, calcified plaque provided more information about the extent of brain changes than traditional ultrasound measures of the presence of plaque in the carotid artery.

The researchers studied 885 people, average age 67, participating in the Rotterdam Study, which includes varying types of imaging to better understand the causes and predictors of dementia and stroke. They used computed X-ray tomography (CT) scans to measure calcification in four blood vessel areas: the coronary arteries that feed the heart; the aortic arch (part of the body's largest artery that delivers blood from the heart into the general circulation); and the extracranial and intracranial carotid arteries that carry blood through the neck into the brain.

Researchers used magnetic resonance imaging or MRI of the brain to visualize small brain infarctions, microbleeds (tiny brain bleeds) and bright areas called white matter lesions. White matter in the brain refers to the fiber tracts that carry information to and from the brain. White matter lesions are more commonly seen in patients who have risk factors such as a history of hypertension, diabetes and high cholesterol.

"These subclinical brain changes, apparent on MRI, do not necessarily cause symptoms right away but are frequently seen in patients with stroke or dementia and over the long term may be associated with worse cognitive performance," Vernooij said.

Among the results:

Calcium build-up in each of the four arteries scanned was associated with the presence of small brain infarctions and white matter lesions in the brain.
No associations were found between microbleeds in the brain and calcification in any of the arteries studied.
As predicted, the amount of calcification in vessels closer to the brain — the extracranial and intracranial carotids — had the strongest relationship to MRI markers of vascular brain disease.
The most prominent associations were found between intracranial carotid calcification and the volume of white matter lesions, and extracranial carotid calcification and brain infarctions.
"The distinction between the impact of calcification in the extracranial and intracranial carotids adds to the current belief that white matter lesions mainly result from disease in smaller intracranial vessels, while brain infarctions are thought to be mainly caused by larger vessel disease," Vernooij said.

The results will be used to advance the understanding of how atherosclerosis affects brain function and ultimately the risk of developing dementia and stroke.

"We are a long way from using CT-assessed calcification to screen individuals for brain lesions and dementia risk," Vernooij said.

Unanswered questions include whether treatment can reduce calcification in blood vessels and whether doing so would improve cognitive health or lower the risk of dementia and stroke.

However, if a physician has performed a heart CT scan to assess heart attack risk, the results may provide information that extends beyond the reason for the examination.

"Though far away from the brain, calcification in coronary arteries may indicate the presence of subclinical brain disease as well," Vernooij said.

Co-authors are: Daniel Bos, M.D.; M. Arfan Ikram, M.D., Ph.D..; Suzette E. Elias-Smale, M.D., M.Sc.; Gabriel P. Krestin, M.D., Ph.D.; Albert Hofman, M.D., Ph.D.; Jacqueline C.M. Witteman, Ph.D.; and Aad van der Lugt, M.D., Ph.D. Author disclosures and funding sources are on the manuscript

Thursday, April 28, 2011

Is there a risk of dementia after surgery

AC Content

It is recognized that there is difficulty with mental functioning after surgery in the elderly, according to an article in the June 2003 issue of Clinical Anesthesiology. It now has an official name, which is
post-operative cognitive dysfunction. It is sometimes called POCD. There is limited knowledge on how to predict it and reduce its risk. Local anesthesia can have the same or worse effects as general anesthesia. It has some similarities to other dementias. It has a number of differences as well.

Dementia is a chronic, progressive decrease in the functioning of the brain. The most evident feature is short-term memory loss. Dementia involves other cognitive function problems such as inappropriate behavior, poor judgment, and inability to learn and communicate, think clearly and keep safe. It may be the result of a number of medical conditions, the most common of which is Alzheimer's disease. The symptoms of dementia most often get worse over time, rather than coming on suddenly after an event such as surgery.

Post-operative cognitive dysfunction is a decline in cognitive function that lasts for weeks or months after surgery. It is important because those with it have an increased risk of disease or death. Patients with post-operative cognitive dysfunction at their hospital discharge have a better than average chance of dying in the first three months after surgery, and those with POCD at both discharge and three months are more likely to die in the first year after surgery than those with no POCD, according to an article in the January issue of the journal Anesthesiology. Most people recover from uncomplicated post-operative cognitive dysfunction. Persons do not recover from dementia unless...read all of Dementia risk after surgery

Monday, August 23, 2010

Stress increases dementia risk

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Mid-life stress can increase the risk of women developing Alzheimer's disease, a study has shown.

Women who reported repeated episodes of stress and anxiety in middle age were up to twice as likely to develop dementia than those who did not, a team of Swedish scientists found.

The majority of those affected were diagnosed with Alzheimer's, the most common form of dementia.

Researchers followed the progress of 1,415 women between 1968 and 2000.

Three surveys in 1968, 1974 and 1980 were carried out to assess levels of psychological stress experienced by the women, who were aged between 38 and 60 at the start of the study.

Stress was defined as a "sense of irritation, tension, nervousness, anxiety, fear or sleeping problems" lasting a month or more.

During the course of the study, 161 of the women taking part developed dementia, mainly in the form of Alzheimer's disease.

Dementia risk was 65% higher in women who suffered frequent stress in middle age. The chances of developing dementia increased as women responded to more than one survey by saying they were frequently stressed.

The risk increased by 73% when women reported frequent or constant stress on two occasions, and more than doubled when all three surveys showed they were stressed.

The findings were published in the journal Brain.

Tuesday, May 11, 2010

MENTAL ILLNESS: Spouses of dementia patients more likely to develop the illness, too

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Here is a dementia music activity

Compiled from reports by Free Press news services

Previous PageMarried adults who have a spouse with dementia are much more likely themselves to develop dementia, according to a study published last week in the Journal of the American Geriatrics Society.

The study suggested that either the stress of being a caregiver or something about the shared environment of the couple contributes to the second case of dementia.
Researchers from Utah examined 2,442 married people ages 65 and older, none of whom had dementia at the start of the study. They were monitored for 12 years.
During that time, 125 cases of dementia were diagnosed in husbands and 70 cases in wives and 30 cases in which both the husband and wife were diagnosed. The analysis showed that people with a spouse with dementia had a six times higher risk of developing dementia themselves. The risk, however, was much higher for men caring for their wives than for wives caring for their husbands.
"On the positive side, the majority of these individuals with spouses who develop dementia did not themselves develop dementia," said lead author of the study, Dr. Maria Norton of Utah State University

More on MENTAL ILLNESS: Spouses of dementia patients more likely to develop the illness, too

Friday, November 6, 2009

Judicious Drinking Associated with Reduced Risk of Dementia

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medpageToday

By John Gever, Senior Editor, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco .

MAYWOOD, Ill., Having a drink only occasionally may reduce the risk of dementia, perhaps because long exposure to low alcohol levels help brain cells survive other stresses, researchers here said.

Most studies that have sought to compare drinking patterns with risk factors associated with dementia have found that moderate drinkers generally have a lower risk, according to Michael A. Collins, Ph.D., of Loyola University Chicago, and colleagues.

Yet their literature review of cardiovascular and neurological effects of ethanol, published online in Alcoholism: Clinical and Experimental Research, outlined a potential neuroprotective mechanism that light-to-moderate drinking could induce.

It was derived from a variety of preclinical studies of a phenomenon known as alcohol preconditioning.

In an interview, Dr. Collins said it was analogous to ischemic preconditioning, in which exposing brain neurons to a brief period of hypoxia helps them survive later bouts of more severe ischemia, such as would occur in a stroke.

These studies have shown that neurons in vitro temporarily dosed with low levels of ethanol can survive stresses that kill untreated neurons.

Dr. Collins said the mechanism appears to involve a sensor-transducer pathway, in which focal adhesion kinase and certain protein kinase C species are activated following low-dose alcohol exposure, which in turn generates two heat shock proteins, Hsp27 and Hsp70.

These latter proteins are well-known to protect cells from stress.

The likelihood of a direct neuroprotective mechanism is boosted by laboratory studies with two known neurotoxic agents, gp120 and beta-amyloid protein. The latter is believed to play a role in Alzheimer's disease, while gp120 is responsible for HIV dementia.

Pretreatment with alcohol protected brain neurons from these agents in vitro, Dr. Collins said.

Whether the preconditioning model accurately reflects what goes on in the brains of human drinkers is uncertain, Dr. Collins acknowledged.

"It is nonetheless conceivable that light-to-moderate, stable alcohol ingestion over years exerts 'preconditioning-like' effects on glia and neurons," he and his colleagues wrote in their review.

Noting that millions of new cases of dementia are diagnosed annually, they added, "it seems imperative that as much as possible is learned about the apparent cytoprotective mechanisms engendered by low-moderate alcohol intake and levels."

The review covered more than 100 studies of the cardiovascular and neurological effects of ethanol. It summarized and updated the proceedings of a roundtable meeting organized and chaired by Dr. Collins in 2007.

Dr. Collins and colleagues noted that not all studies showed a decreased risk. Moreover, they said, many of the investigators who did find reduced risk factors attributed their findings to the hematologic and cardiovascular effects of alcohol, or of other components of alcoholic drinks such as resveratrol.

But the review also included a number of in vitro and animal studies suggesting that low-dose ethanol has direct neuroprotective effects.

"Light to moderate, non-binge alcohol intake . . . does no apparent harm to cognition during aging, even possibly reducing the risk of cognitive decline [and] dementia," Dr. Collins and colleagues said.

"Alcohol-related anti-inflammatory heat shock protein and protein kinase changes in the brain bear similarities to those elucidated in the heart, particularly with respect to protein kinase C and quite likely other signal transduction kinases," they added