Showing posts with label cognitive decline. Show all posts
Showing posts with label cognitive decline. Show all posts

Friday, March 23, 2018

Is high cholesterol beneficial in older adults

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The Mount Sinai Health System

People over 85, with a cholesterol increase, showed less decline in cognition and thinking. Should we stop our statins and change our diets? 




People aged 85 and older whose total cholesterol had increased from their levels at midlife had a reduced risk for marked cognitive decline, compared with those a decade younger whose cholesterol was similarly elevated, Mount Sinai researchers report in a new study. 

The results of the study appear in Alzheimer's & Dementia: The Journal of the Alzheimer's Association. The researchers found that people aged 85-94 with good cognitive function whose total cholesterol increased from midlife had a 32 percent reduced risk for marked cognitive decline over the next ten years, compared with people aged 75-84, who had a 50 percent increased risk. 


Increase Our Cholesterol?

The researchers said that the results did not suggest that those 85 and older should increase their cholesterol for better cognitive health, but rather that those in that age cohort with good cognition and high cholesterol probably also had some protective factor that someday could be identified and studied. 

The research team evaluated the association of five total cholesterol values with a substantial decline in cognitive function from normal function, called marked cognitive decline. The five values were midlife (average age 40) total cholesterol, late-life (average age 77) total cholesterol, mean total cholesterol since midlife, linear change since midlife (in other words, whether it was increasing or decreasing), and quadratic change since midlife (whether the linear change was accelerating or decelerating). Data were obtained from the original Framingham Heart Study, a long-term, ongoing cardiovascular cohort study on residents of Framingham, Massachusetts. That study began in 1948 with 5,209 adult subjects and is now on its third generation of participants

Over 85, Under 75

The team assessed whether marked cognitive decline was associated with the five cholesterol values, and whether the associations with those values changed depending on the age of cognitive assessment. They found several cholesterol values including high last cholesterol, increasing levels, and decreasing acceleration were predictors associated with increased risk of a marked cognitive decline, that were associated with increased risk of a marked cognitive decline. However, as the outcome age increased, some associations were reduced, or even reversed. Furthermore, in the subgroup of cognitively healthy 85-94 year olds, a high midlife cholesterol level was associated with a reduced risk for marked cognitive decline. This contrasts with samples in other studies that have focused on elderly subjects primarily below age 75, where midlife cholesterol was associated with increased risk of cognitive decline.

Successful Cognitive Aging

"Our results have important implications for researching genetic and other factors associated with successful cognitive aging," said the study's first author, Jeremy Silverman, PhD, Professor of Psychiatry, Icahn School of Medicine at Mount Sinai. "The data are consistent with our protected survivor model - among individuals who survive to very old age with intact cognition, those with high risk factor levels are more likely to possess protective factors than those with lower risk factor levels. Long-lived individuals who are cognitively intact despite high risk should be targeted in research studies seeking protective factors, which could help identify future drugs and therapies to treat dementia and Alzheimer's disease." 

Dr. Silverman notes that these results do not imply that those 85 and older should increase their cholesterol. His research team will next study other risk factors for cognitive decline, including body mass index and blood pressure.. 

"We don't think high cholesterol is good for cognition at 85, but its presence might help us identify those who are less affected by it. We hope to identify genes or other protective factors for cogitive decline by focusing on cognitively healthy very old people who are more likely to carry protective factors."


SOURCE:
  • The Mount Sinai Health System is New York City's largest integrated delivery system encompassing seven hospital campuses, a leading medical school, and a vast network of ambulatory practices throughout the greater New York region. For more information, visit http://www.mountsinai.org


Thursday, April 12, 2012

Eli Lilly Says FDA Approved Alzheimer's Diagnostic Agent Amyvid

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RTT News

Eli Lilly and Company (LLY: News ) on Friday said the Food and Drug Administration (FDA) has approved Amyvid, a radioactive diagnostic agent for use in patients being evaluated for Alzheimer's Disease and other causes of cognitive decline.

Amyvid or florbetapir F 18 injection is a molecular imaging agent under investigation for the Positron Emission Tomography imaging of beta-amyloid plaque in the brains of Alzheimer's disease patients.

A negative Amyvid scan indicates sparse-to-no amyloid plaques are present, which is inconsistent with a neuropathological diagnosis of Alzheimer's Disease and reduces the likelihood that a patient's cognitive impairment is due to Alzheimer's Disease.

A positive scan indicates moderate to frequent amyloid plaques are present. This amount of amyloid plaque is present in patients with Alzheimer's Disease, but may also be present in patients with other types of neurologic conditions and in older people with normal cognition.

Amyvid was a lead candidate of Avid Radiopharmaceuticals, which became a wholly owned subsidiary of Lilly through its acquisition by the Indianapolis, Indiana-based health care giant in December 2010.

Friday, December 30, 2011

Small brain cortex may mean early dementia

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By RICK NAUERT PHD Senior News Editor
Reviewed by John M. Grohol, Psy.D.
Size may matter in predicting the chance for Alzheimer’s disease as new research suggests an association between the size of various brain regions and the risk for very early Alzheimer’s disease.

The study suggests people with smaller regions of the brain’s cortex may be at risk.

Researchers have published their findings in the online issue of Neurology®, the medical journal of the American Academy of Neurology.

“The ability to identify people who are not showing memory problems and other symptoms but may be at a higher risk for cognitive decline is a very important step toward developing new ways for doctors to detect Alzheimer’s disease,” said Susan Resnick, Ph.D.

For the study, researchers used brain scans to measure the thickness of regions of the brain’s cortex in 159 people free of dementia with an average age of 76.

The brain regions were chosen based on prior studies showing that they shrink in patients with Alzheimer’s dementia.

Of the 159 people, 19 were classified as at high risk for having early Alzheimer’s disease due to smaller size of particular regions known to be vulnerable to Alzheimer’s in the brain’s cortex, 116 were classified as average risk and 24 as low risk.

Investigators tested subjects at the beginning of the study and over the next three years. Researchers administered tests that measured memory, problem solving and ability to plan and pay attention.

The study found that 21 percent of those at high risk experienced cognitive decline during three years of follow-up after the MRI scan, compared to seven percent of those at average risk and none of those at low risk.

“Further research is needed on how using MRI scans to measure the size of different brain regions in combination with other tests may help identify people at the greatest risk of developing early Alzheimer’s as early as possible,” said study author Bradford Dickerson, MD.

Researchers also discovered that 60 percent of the group considered most at risk for early Alzheimer’s disease had abnormal levels of proteins associated with the disease in cerebrospinal fluid — which is another marker for the disease — compared to 36 percent of those at average risk and 19 percent of those at low risk.

Source: American Academy of Neurology

Thursday, November 10, 2011

Sleep Disorders Lead To Increased Dementia Risk

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openPR

Older women with sleep-disordered breathing are more likely to develop cognitive impairment or dementia than women without this disorder according to a new study.

According to medical researchers, sleep-disordered breathing is a condition where the person has recurrent arousals from sleep and intermittent hypoxemia. "This condition can be common among older people and affects up to 60 percent of the elderly population," explains Jesse Slome, director of the American Association for Long Term Care Insurance.

Health experts report that the condition has been linked to various adverse health problems including hypertension, cardiovascular disease and diabetes. Researchers at the University of California, San Francisco, investigated the link between prevalent sleep-disordered breathing measured and the subsequent diagnoses of mild cognitive impairment and dementia.

The study tested nearly 300 women who were the average age of 82.3 years. The participants were without dementia at the start of the study. The participants' cognitive status was ranked as normal, dementia, or mild cognitive impairment. The study examined measures of hypoxia, sleep fragmentation and sleep duration as underlying mechanisms for any link between sleep-disordered breathing and cognitive impairment.

According to the study, some 35.2 percent of the tested women met the criteria for sleep-disordered breathing. Nearly an equal amount, some 35.9 percent of the women, developed mild cognitive impairment (20.1 percent) or dementia (15.8 percent) after an average follow up of 4.7 years. The study revealed, 47 of women (44.8 percent) with sleep-disordered breathing acquired mild cognitive impairment or dementia in comparison with 31.1 percent of those without sleep-disordered breathing.

Cognitive decline and dementia is a leading reason that aging senior women ultimately require costly long term care, Slome acknowledges. "Long term care insurance can pay for qualifying care at home or in a skilled nursing home but you must apply well before a decline in mental ability or physical health takes place," he notes.

Thursday, August 4, 2011

Success: Smell Test for Cognitive Decline

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WebMD

Researchers Report Early Success With Smell Test for Cognitive Decline

Australian researchers say they’re a step closer to developing a simple smell test that may help predict which older adults will develop cognitive impairment and Alzheimer's disease.

The work is still very preliminary. But it appears that people who have memory loss and other signs of mental decline that can lead to Alzheimer's may have trouble discriminating between smells, says study leader Hamid R. Sohrabi, PhD, a neuropsychologist at Edith Cowan University in Perth, Australia.

William Thies, PhD, chief medical and scientific officer at the Alzheimer’s Association, tells WebMD that animal and lab research suggests there is an association between cognitive decline and smell, but that efforts to develop a commercial test have failed to date.

"It's not too surprising that the sense of smell changes, as the amyloid plaques and tangles that are thought to cause Alzheimer's develop in the same area of the brain that houses our olfactory pathway," he says.

The Sniffin' Stick Test
To determine whether cognitive impairment is associated with trouble smelling, Sohrabi and colleagues studied 308 people aged 46 to 86 with no memory problems.

All were given the "Sniffin' Stick" test, in which a person is presented three sticks, two of which have the same odor. Then he or she needs to pick out the one with the different odor. If the wrong stick is identified, the test is repeated with a slightly higher concentration of the odor, for a total of up to 16 times.

Over the next three years, 58 participants showed signs of cognitive decline, as determined by worsening scores on a simple questionnaire called CAMCOG that is used to assess memory and assist in the diagnosis of Alzheimer's.

Results showed that participants who had more trouble distinguishing between smells at the start of the study were more likely to shows signs of mental decline.

The analysis took into account other factors that can affect memory loss, such as age, sex, and education.

The findings were presented here at the Alzheimer's Association International Conference 2011.

Sohrabi says he hopes that test can be refined and someday be used to detect Alzheimer's disease early, before symptoms develop.

Other tests are further along in development, but none yet ready for clinical use.

"There is a long way to go,” Thies says. “You have to figure out which odor is best, test it in hundreds of people and validate it and then standardize the test so results are the same from one place to the next.”

Other tests are further along in development. These include tests that look for changes in the blood and cerebrospinal fluid that have been linked to the amount of Alzheimer's-associated plaque in the brain and an experimental test that looks for changes in the eye that can precede the development of Alzheimer's.

These findings were presented at a medical conference. They should be considered preliminary as they have not yet undergone the "peer review" process, in which outside experts scrutinize the data prior to publication in a medical journal.

Saturday, January 8, 2011

Long-Term Pesticide Exposure Linked to Cognitive Decline

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Medscape Today
Megan Brooks

Individuals exposed to pesticides on the job are more likely than their unexposed peers to experience a decline in cognitive function as they grow older, new research shows.




"The mild impairment we observed raises the question of...possible evolution towards neurodegenerative diseases such as Alzheimer's disease or other dementias," write Isabelle Baldi, MD, from the Université Victor Ségalen Bordeaux 2 in Bordeaux, France, and colleagues.



The study was published online December 2 in Occupational and Environmental Medicine.



Despite growing evidence linking pesticide exposure to neurological diseases, epidemiological data on neurobehavioral effects of chronic pesticide exposure are limited, the study team notes.



The PHYTONER study is monitoring the neurobehavioral effects of long-term exposure to pesticides in vineyard workers in southwest France. A total of 929 workers aged between 42 and 57 years enrolled in the study between 1997 and 1998.



Dr. Baldi's team followed-up with 614 study participants between 2001 and 2003. On both occasions, the workers completed a questionnaire and 9 neurobehavioral tests that measured memory and recall skills, language retrieval skills, verbal skills, and reaction time.



All of the participants have worked in agriculture for at least 20 years. They were grouped into 4 categories of on-the-job pesticide exposure: directly exposed (mixing or applying pesticides, cleaning or repairing spraying equipment; n = 336), certainly indirectly exposed (contact with treated plants; n = 107), possibly indirectly exposed (work in building, offices, cellars; n = 52), and not exposed (none of the above; n = 119). The analysis did not focus on specific pesticides.



On both testing occasions, lower scores in some or all of the cognitive tests were associated with older age, lower education levels, excessive alcohol intake, depression, and drug use, which was not unexpected, the researchers note.



In follow-up testing, the risk for scoring low on a cognitive test was higher in exposed subjects, with odds ratios ranging from 1.35 to 5.60.



In addition, when the authors compared baseline test scores with follow-up test scores 4 to 5 years later, they found that exposed workers had the greatest decrease in performance with time.



In all but 2 of the tests, those who had been exposed to pesticides were most likely to perform worse the second time around compared with nonexposed workers.



In multivariate analysis taking into account the type of exposure, the odds ratio for a 2-point drop on the Mini-Mental State Examination between baseline and follow-up was 1.97 (95% confidence interval, 1.09 - 3.59) in the directly exposed workers compared with the nonexposed workers.



"This result is particularly striking in view of the short duration of follow-up and the relatively young age of the participants," Dr. Baldi and colleagues write.



They point out that no decline in MMSE scores was seen over the course of 5 years in a separate longitudinal study of cognitive test performance in a general, dementia-free French population aged 65 years and older.



"The observed decline in pesticide-exposed subjects on the MMSE, a composite measure reflecting global cognitive deterioration, cannot therefore be considered a sole effect of ageing, especially since the subjects were relatively young," they say.



The current findings, Dr. Baldi and colleagues say, are consistent with several previous studies in pesticide-exposed farm workers. In addition, in a recent review of 21 relevant studies on the cognitive effects of chronic pesticide exposure, 76% found positive associations with some tests, and 82% found a relationship with psychomotor function (Kamel et al. Environ Health Perspect. 2004).



In correspondence with Medscape Medical News, Dr. Baldi said the second follow-up of the PHYTONER cohort began this year, a full 12 years after baseline. This time lag, she said, should provide a better understanding of cognitive impairment and its evolution in pesticide-exposed vineyard workers. It is also possible that the first cases of Alzheimer's disease among the study group will be identified, as they will be close to 65 years old.

The study is supported by the Ministère de l'Environnement, Agence Nationale pour l'Amélioration des Conditions de Travail, Conseil Régional d'Aquitaine, Recherche et Partage. The authors have disclosed no relevant financial relationships.

CME Education online




Friday, September 10, 2010

Mental Stimulation Postpones, Then Speeds Dementia (part 2)

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Allison Augbry

His(Yaakov Stern) theory is that mentally engaged people build up a "cognitive reserve" that may help them compensate when the initial brain changes associated with dementia and Alzheimer's begin to develop.

"One simple idea is that perhaps they have more flexibility in how they approach tasks," Stern says. So, if the disease begins to disrupt or damage one network in the brain, they may be able to engage alternative networks in the brain to solve problems or do tasks.

Delay Followed By Speedy Decline

So for those who are mentally engaged, it may take many more years for the symptoms of the disease to appear. But once they do, the course of the disease seems to speed up. Researchers say there's a bit of a silver lining here: knowing that the disease will likely progress more quickly.

"We think this is very good news," Wilson says. "It suggests that cognitive activity extends your period of cognitive independence as long as it possibly can."

And it will likely shorten the battle at the end of life. This means Alzheimer's patients may be less of a burden to caregivers and loved ones.

Wednesday, September 8, 2010

Mental Stimulation Postpones, Then Speeds Dementia

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Allison Augbry

When it comes to staving off dementia, new evidence suggests that the "use it or lose it" dictum holds true — at least for a while. But it also appears that mentally stimulating lifestyles may speed up dementia once it hits in old age.

"We do think that a cognitively active lifestyle is protective up to some point," says Robert Wilson, a professor of neurological sciences at Rush University Medical Center in Chicago.

But the protection doesn't hold up indefinitely.

New Evidence

Wilson and his colleagues recruited 1,157 people age 65 and older from the Chicago area. When the study began, none of the seniors had dementia. During face-to-face interviews, each was asked how often he or she participated in stimulating activities. "Things such as reading a newspaper, listening to the radio, going to a museum, or playing a board game such as chess or checkers," Wilson says. Then they gave each person a score on a cognitive activity scale. The more frequently people engaged in stimulating activities, the higher their score.

More than a decade later, researchers followed up with cognitive evaluations and diagnostics. They found that among the seniors who didn't have dementia, the rate of cognitive decline was reduced by 52 percent for each point on the cognitive activity scale. But the results were much different for those who developed Alzheimer's disease — their rate of decline increased. The average rate of decline per year increased by 42 percent for each point on the cognitive activity scale.

Findings Fit With Theory Of 'Cognitive Reserve'

"Someone who's brilliant and engages in a lot of activities might reduce their risk of Alzheimer's disease for a while," says Yaakov Stern, professor of clinical neuropsychology at Columbia University

His theory... come back to dementia views soon to see

Saturday, August 21, 2010

Direct Relationship Seen Between Plasma Aβ Levels and Cognitive Decline (part 3)

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Pam Harrison (Medscape Today)

Relatively Rapid Decline

As the authors point out, the relatively rapid cognitive decline seen as a function of high baseline plasma Aβ levels and stable or decreasing Aβ42 in the entire sample is not surprising given that a similar plasma Aβ profile predicted conversion to Alzheimer's disease in the same sample in an earlier study — cognitive decline in more than one domain is a prerequisite for incident Alzheimer's disease.

"We need to further validate these Aβ levels, and we also need to understand how plasma Aβ levels relate to brain levels," Dr. Cosentino cautioned. "But once we have a better understanding of this, testing patients for plasma Aβ levels is an inexpensive and noninvasive way to identify people at greater risk for cognitive decline and Alzheimer's disease, and ultimately, this would be very important in terms of being able to provide preventive treatment when we have such a treatment."

The study was supported by grants from the National Institutes of Health. The authors have disclosed no relevant financial relationships.

Thursday, August 19, 2010

Direct Relationship Seen Between Plasma Aβ Levels and Cognitive Decline (part 2)

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Pam Harrison (Medscape Today)

Aging Project

The amyloid cascade hypothesis suggests that Alzheimer's disease develops subsequent to aberrant metabolism of glycoproteins, the precursors to amyloid, the authors write. Aβ40 and Aβ42 then accumulate, and this accumulation is considered the primary trigger for the development of Alzheimer's disease. Previous research indicates that plasma Aβ levels decrease as brain levels increase, suggesting that plasma Aβ level may be used as a biomarker of disease risk.

In this study, participants were drawn from the Washington Heights and Inwood Columbia Aging Project and represented 3 broadly defined ethnic groups: Caribbean Hispanic, black, and white. All participants were free of dementia at the time of the first Aβ sample; at follow-up, 481 patients remained cognitively healthy, 329 were cognitively or functionally impaired but not demented at any point, and 70 developed Alzheimer's disease.

Investigators then determined whether Aβ levels could be linked to either specific cognitive changes that constitute conversion to Alzheimer's disease or whether they corresponded to cognitive change independent of dementia. Cognitive change consisted of a composite score and memory, language, and visuospatial indices.

When researchers examined cognitive change in specific domains by Aβ, they determined that baseline Aβ42 predicted cognitive change in all 3 domains in the overall sample, with those in the highest Aβ quartile "consistently declining faster" than those in the lowest. "Baseline Aβ40 quartile predicted change in memory," the authors add, with those in the second and third quartiles declining faster than those in the lowest quartile.

Baseline Aβ40 quartiles also predicted change in language, with individuals in the highest quartile declining faster than those in the lowest. "Finally, change in Aβ42 predicted change in memory and visuospatial scores, with relatively stable or decreasing Aβ42 predicting faster decline," the researchers add. Among the group who remained cognitively healthy during the study interval, baseline Aβ42 predicted change primarily in memory, with higher baseline levels generally predicting faster decline.

In contrast, baseline Aβ40 was generally unrelated to cognitive change in the same healthy elderly group, and change in Aβ42 was not associated with change in any domain. Finally, change in Aβ40 over time was not related to cognitive change in either the overall sample or the cognitively healthy.

Relatively Rapid Decline

As the authors point out, the relatively rapid cognitive decline seen as

Tuesday, August 17, 2010

Direct Relationship Seen Between Plasma Aβ Levels and Cognitive Decline

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Pam Harrison (Medscape Today)

There is a direct and linear association between plasma beta-amyloid (Aβ) levels and multiple aspects of cognitive decline over time, including cognitive changes that constitute conversion to Alzheimer's disease, according to new findings from a population-based, ethnically diverse longitudinal sample of older adults.

Stephanie Cosentino, PhD, from the Taub Institute for Research in Alzheimer's Disease and the Aging Brain at Columbia University Medical Center, New York City, and multicenter colleagues found that in their overall sample of 880 adults, individuals in the top 3 quartiles of Aβ42 at baseline had faster declines in cognitive function during 4.5 years of follow-up than those in the lowest quartile. The same observation held largely true for individuals who remained cognitively healthy during the same study interval.

"Individuals in the top 3 Aβ40 quartiles also declined faster than those in the lowest quartile," investigators add, "[whereas] in the healthy elderly individuals, only the highest quartile declined faster than those in the lowest."

Looking at the rate of global cognitive change by change in Aβ, investigators noted that in both the overall cohort and the healthy elderly, individuals with relatively stable or decreasing Aβ42 values had faster cognitive decline than those with increasing Aβ42 values.

In contrast, change in Aβ40 was not associated with cognitive change in either the overall cohort or the healthy elderly.

"What we tend to see in healthy elders is a steady increase in Aβ42 levels over time, so what we are trying to characterize here is the absence of an increase," Dr. Cosentino told Medscape Medical News.

She also noted that previous studies have shown that high initial plasma levels of Aβ and declining levels of Aβ over time are risk factors for Alzheimer's disease, "so changes in Aβ levels provide information about disease risk." In this particular study, changes in the same plasma Aβ levels predicted the rate of cognitive decline in patients who eventually developed dementia.

"This linear association between plasma Aβ and cognitive change increases our ability to use plasma Aβ as a marker of impending cognitive decline and Alzheimer's disease," Dr. Cosentino said, adding that interestingly enough, the same Aβ profile predicted cognitive decline even in those individuals who remained healthy over time.

The study was published online August 9 and will appear in the December issue of the Archives of Neurology.

Aging Project

The amyloid cascade hypothesis suggests that

Thursday, August 5, 2010

Diet and Behavior Changes May Slow Alzheimer’s

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US News and World Report

By Gwyneth Dickey, Science News

A combination of diet and lifestyle changes decreases Alzheimer’s-like symptoms in dogs more than either treatment does on its own, a new study shows. The findings show the importance of taking multiple approaches to arrest the disease in humans, the authors say. Their results also provide evidence supporting recent research that suggests plaque deposits in the brain are not the cause of Alzheimer’s.


Alzheimer’s disease usually strikes people over the age of 60 and causes memory loss, shrinking brain tissue and eventually death. People with the disease get plaques in their brains made up of a small protein called amyloid-beta, which clumps together and disrupts brain signals.

Research suggests diet and exercise can improve human brain function and defend against Alzheimer’s, but researchers aren’t sure why. Dogs naturally accumulate the same brain plaque, and though they don’t get Alzheimer’s, they do experience age-related cognitive decline. So scientists can study the animals to learn more about the human form of the disease.

In this study, 24 beagles 8 to 12 years old received one of four treatments over about 2 ½ years. Some dogs were fed a diet enriched with high-antioxidant foods, like spinach, tomatoes, grapes, carrots and citrus fruit. Other dogs were given behavioral enrichment, in which they socialized with other dogs, played with new toys, took long walks and learned new tasks. One group of dogs received both treatments, while the last group received none.

This is the first study to look at antioxidant and behavioral enrichment treatments in dogs that naturally accumulate amyloid-beta plaques, says neuroscientist Viorela Pop, who conducted the research as a graduate student at the University of California, Irvine. The results were published July 21 in the Journal of Neuroscience.

The researchers found that compared with controls, dogs given the combined treatment had the greatest benefit. Those dogs had the biggest improvement in cognition and moderately reduced plaques in their brains. Dogs given just antioxidants fared better than dogs that underwent only enrichment activities. “The combination treatment is a key component of this study,” says Pop, who is now a postdoctoral fellow at Loma Linda University in California. “If we were to try to slow down Alzheimer’s disease in humans, we would want to try a multifactorial treatment.”

Her study also adds to a growing body of research that suggests amyloid-beta plaques, once thought to be the cause of Alzheimer’s, are just a symptom of the disease. Beagles receiving both dietary and behavioral treatments showed major improvements in cognition, but only minor decreases in amyloid-beta plaques in their brains.

The results fit with evidence showing that humans and dogs immunized against amyloid-beta plaques have no clumps but continue to experience cognitive decline, says Alex Roher of the Banner Sun Health Research Institute in Sun City, Ariz. “Patients continue to deteriorate in spite of all treatments, which tells you the plaques are not the ultimate cause of the disease.”

That’s not to say amyloid-beta isn’t important. “It just doesn’t seem to be the main thing responsible for cognitive decline in dogs and Alzheimer’s disease in humans,” Pop says.

Researchers need to conduct more studies before these results can be generalized to humans, says psychologist Catherine Roe of the Washington University School of Medicine in St. Louis. “Going from dogs to people is a big jump,” she says, and researchers need to find links between enriched diet and environment in humans. “So far we haven’t found any association.”

---

Wednesday, September 30, 2009

Impaired Kidney Function Linked To Cognitive Decline In Elderly

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ScienceDaily — A new study published in the medical journal Neurology suggests that impaired kidney function is a risk factor for cognitive decline in old age


The study, conducted by researchers at Rush University Medical Center, found that poor kidney function was linked specifically with cognition related to memory functions. Damage to one of these functions, episodic memory, which retrieves memories of time, place, associated emotions and other contextual knowledge, is often the earliest sign of Alzheimer's disease.

"Given the dearth of modifiable risk factors for age-related cognitive decline, these results have important public health implications," said Dr. Aron Buchman, a neuroscientist in the Rush Alzheimer's Disease Center. "Further work to understand the link between kidney function and the brain may provide new strategies for preventing memory loss in elders."

Buchman said the findings suggest that there are common disease processes that affect both the brain and the kidneys in the elderly, and hypothesized that underlying vascular problems, such as diabetes and hypertension, may account for the association between kidney problems and cognitive decline.

The study analyzed data for 886 older adults who participated in the Rush Memory and Aging Project, a group of community-dwelling seniors with a mean age of 81, all of them initially free of dementia. The participants were examined annually for up to six years to track changes in cognition over time. Cognitive assessments included multiple tests that were summarized as a composite measure of overall cognition and of five individual cognitive abilities.

The individual cognitive systems assessed were visuospatial ability; perceptual speed, or the ability to quickly and accurately compare letters, numbers, objects, pictures or patterns; semantic memory, related to meaning, understanding and other concept-based knowledge; working memory, which temporarily stores and manipulates information; and episodic memory.

Ruling out the influence of factors like aging and medications, which can affect cognition, the researchers found that poor kidney function, assessed at the beginning of the study, was linked with a more rapid rate of decline in cognition over the next several years – not in visuospatial ability or perceptual speed, but in three specific areas: episodic, semantic and working memory.

The rate of decline in cognition was equivalent to that of a person seven years older at baseline, Buchman said.

The study was supported by funds from the National Institute on Aging, the Illinois Department of Public Health and the Robert C. Borwell Endowment Fund.

Monday, August 10, 2009

Working Overtime May be a Risk for Dementia

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Brain Blogger

By Jennifer Gibson, PharmDcloseJennifer Gibson, PharmD Name: Jennifer Gibson
Site: http://brainblogger.com

Many occupations can make you feel like you are losing your mind, but new evidence suggests that long working hours may actually lead to cognitive decline. Notably, cognitive impairment in midlife is already established as a risk factor for Alzheimer’s Disease and other forms of dementia. A new report from the Whitehall II Study, published in the American Journal of Epidemiology finds that long working hours in midlife are associated with a decline of cognitive function, and possibly dementia.

Earlier studies from the Whitehall Study group and related evaluations reported that long working hours are associated with cardiovascular and immunologic disorders, reduced sleep quality and duration, unhealthy lifestyle choices, and overall adverse health outcomes. Data examining the association between work hours and cognitive function is scarce, but the current study attempted to evaluate the link, since risk factors in midlife are important predictors of dementia in late life. For the cross-sectional study of 248 automotive workers in Britain, participants completed numerous tests related to memory and vocabulary, as well as general health, psychological well being, and physical functioning. People who worked more than 55 hours per week had significantly lower scores on vocabulary and reasoning tests at baseline and follow-up 5 years later, compared with those who worked 35 to 40 hours per week. The results were not changed when confounding factors were considered, including age, sex, marital status, education, occupation, income, and health risk factors.

Similar studies have concluded that...read all of Working Overtime May be a Risk for Dementia

Saturday, May 16, 2009

Eye Disease, Cognitive Decline Linked in Study

ajc

HealthDay News) -- Seniors who perform poorly on tests of language, memory and concentration are more likely to be suffering from the early stages of age-related macular degeneration, a major cause of vision loss, a new study suggests.

The finding stems from a look at the association between cognitive function decline and the onset of age-related macular degeneration (AMD) among approximately 2,000 Australian seniors between the ages of 69 and 97.

"We found that those who have memory impairment were more likely to have early stages of macular degeneration independent of the effects of age, education and vascular risk factors," said study co-author Dr. Tien Yin Wong, a professor in the department of ophthalmology within the Centre for Eye Research Australia at the University of Melbourne.

Wong and his colleagues published the findings in the May issue of the Archives of Ophthalmology.

Age-related macular degeneration is the leading cause of vision loss among the elderly. The researchers note that prior research has suggested that Alzheimer's disease and AMD share similar developmental pathways in terms of protein build-up and brain and eye changes.

The authors' current observations are drawn from an analysis of retinal photographs taken of study participants (more than 80 percent white and all enrolled in a larger cardiovascular health study), from which a diagnosis of early-stage AMD was made.

Those diagnoses were lined up against results of cognitive function and neuropsychological tests designed to assess each subject's abilities in terms of concentration, language, memory and orientation skills. Most were also tested for dementia and cardiovascular risk factors.

The researchers determined that nearly 16 percent of the participants had early AMD, while 135 and 86 patients were diagnosed with dementia or Alzheimer's disease, respectively.

Having dementia and/or Alzheimer's was not linked to an increased likelihood for early AMD. However, the authors found that an AMD diagnosis was associated with having poorer scores on cognitive testing -- a trend deemed small but "significant."

"Our study suggests that....read the whole article

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Friday, October 10, 2008

The DNA diet and dementia

Red Orbit
Posted on: Thursday, 9 October 2008, 03:00 CDT

By Parslow, Virginia

The development of personalised diets tailored to our genes will help us to both maintain health and relieve disease. Current dietary guidelines provide a "one-size fits all" approach that ignores the genetic differences between individuals. However, studies of the interaction of genes and diet are now coming of age as a result of the sequencing of the human, mouse and rat genomes, improved understanding of the mechanisms that underlie chronic inflammation, and new understandings of the ways in which macronutrients and micronutrients interact with our genetic make-up.

Macronutrients and micronutrients influence the metabolic programming of cells and help control homeostasis. But equally important is how any one person's body will use and respond to nutrients, which is driven at least in part by their genetic make- up.

Prof Bruce Ames of the University of California, Berkeley, says that micronutrient deficiencies are widespread and may be a major preventable cause of the diseases of ageing. Ames" theory states diat the degenerative diseases that accompany ageing, such as immune dysfunction, cancer, cognitive decline....read the whole story
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