Exercise Boosts Brain Power In Over 50s

(MedicalNewsToday.com) Over the years, there has been much research on the potential cognitive benefits of exercise on mental performance in older adults. Overall, results have been inconclusive, but a new review takes a fresh look at the data.

As we age, our cognitive prowess tends to take a hit. Finding a way to halt or reduce this decline would make a huge difference to billions of lives.

One potential intervention is exercise, and many researchers have attempted to prove whether or not it can stave off age-related mental decline and neurodegenerative conditions.

Early research and meta-analyses demonstrated strong, positive results. Over recent years, however, published reviews on the topic have not reported such strong effects.

A Fresh Look at Aging and the Brain

According to the authors of the current paper, recently published reviews and meta-analyses have been inconclusive due to their restrictive inclusion criteria. For instance, some focused on just one type of exercise, while others limited their literature search to a narrow date range. The latest review is published this week in the British Journal of Sports Medicine.

The new analysis casts its net wide, looking at aerobic exercise, resistance training (such as weights), multicomponent exercise (including both resistance and aerobic training), tai chi, and yoga.

To fully assess the impact of these interventions, they looked at a raft of cognitive parameters. These include:

  • Brain capacity – global cognition
  • Attention – sustained alertness, including speed of information processing
  • Executive function – including goal-oriented behaviors
  • Memory – storage and retrieval
  • Working memory – the part of short-term memory that deals with immediate conscious perceptual and language processing

The team’s analysis showed that exercise improved the brain power of people aged 50 and older, regardless of their current brain health.

Prescribing Exercise

The results suggested that aerobic exercise enhanced cognitive abilities, while resistance training had a positive influence on executive function, memory, and working memory. According to the researchers, the results were strong enough to recommend prescribing both exercise types to bolster brain health in over 50s.

The next question asks how much exercise is needed. According to the analysis, a session of moderate to vigorous intensity lasting between 45 and 60 minutes was beneficial to brain health. In fact, any frequency had positive effects.

The authors conclude that:

“The findings suggest that an exercise program with components of both aerobic and resistance type training, of at least moderate intensity and at least 45 minutes per session, on as many days of the week as possible, is beneficial to cognitive function in adults aged over 50 years.”

Interestingly, tai chi was also found to improve cognitive capabilities. This is important because, as a low-impact exercise, it can be carried out by people who could not physically cope with more intense regimes. However, the authors point out that this conclusion was based on only a small number of studies, making the finding less robust.

How Exercise Might Reduce Cognitive Decline

Although there is a great deal of debate on this topic, scientists believe that there are a number of ways that exercise could help to stave off dementia and other degenerative neurological conditions.

According to the authors of the study, these include the promotion of neurogenesis (growth of new nervous tissue), angiogenesis (growth of new blood vessels), synaptic plasticity (the ability of synapses to strengthen or weaken over time), decreased pro-inflammatory processes, and reduced cellular damage due to oxidative stress.

Although the results will be widely heralded as positive, the authors note certain limitations to the study. For example, the analysis was limited to studies that looked at supervised exercise, and only those that were published in the English language.

If physical exercise really can stave off cognitive decline, it will benefit the population at large. This type of intervention can, of course, be cost effective or even free. If it has large-scale benefits, it could be a simple way of improving the lives of millions of older adults.

Even though the cognitive benefits may be small, the physical benefits of exercise are well established – so it is a win-win situation either way.

Citation

http://www.medicalnewstoday.com/articles/317087.php

By Tim Newman

© 2004-2017 All rights reserved. MNT is the registered trademark of Healthline Media.

 

FDA Approves First Consumer Tests for Alzheimer’s Genetic Risk Information

(FDA.gov) The U.S. Food and Drug Administration today allowed marketing of 23andMe Personal Genome Service Genetic Health Risk (GHR) tests for 10 diseases or conditions. These are the first direct-to-consumer (DTC) tests authorized by the FDA that provide information on an individual’s genetic predisposition to certain medical diseases or conditions, which may help to make decisions about lifestyle choices or to inform discussions with a health care professional.

“Consumers can now have direct access to certain genetic risk information,” said Jeffrey Shuren, M.D., director of the FDA’s Center for Devices and Radiological Health.

“But it is important that people understand that genetic risk is just one piece of the bigger puzzle, it does not mean they will or won’t ultimately develop a disease.”

The GHR tests are intended to provide genetic risk information to consumers, but the tests cannot determine a person’s overall risk of developing a disease or condition. In addition to the presence of certain genetic variants, there are many factors that contribute to the development of a health condition, including environmental and lifestyle factors.

The 23andMe GHR tests work by isolating DNA from a saliva sample, which is then tested for more than 500,000 genetic variants. The presence or absence of some of these variants is associated with an increased risk for developing any one of the following 10 diseases or conditions:

The FDA reviewed data for the 23andMe GHR tests through the de novo premarket review pathway, a regulatory pathway for novel, low-to-moderate-risk devices that are not substantially equivalent to an already legally marketed device. Along with this authorization, the FDA is establishing criteria, called special controls, which clarify the agency’s expectations in assuring the tests’ accuracy, reliability and clinical relevance. These special controls, when met along with general controls, provide reasonable assurance of safety and effectiveness for these and similar GHR tests.

In addition, the FDA intends to exempt additional 23andMe GHR tests from the FDA’s premarket review, and GHR tests from other makers may be exempt after submitting their first premarket notification. A proposed exemption of this kind would allow other, similar tests to enter the market as quickly as possible and in the least burdensome way, after a one-time FDA review.

“The special controls describe the testing that 23andMe conducted to demonstrate the performance of these tests and clarify agency expectations for developers of other GHRs,” said Dr. Shuren.

“By establishing special controls and eventually, a premarket review exemption, the FDA can provide a streamlined, flexible approach for tests using similar technologies to enter the market while the agency continues to help ensure that they provide accurate and reproducible results.”

Excluded from today’s marketing authorization and any future, related exemption are GHR tests that function as diagnostic tests. Diagnostic tests are often used as the sole basis for major treatment decisions, such as a genetic test for BRCA, for which a positive result may lead to prophylactic (preventative) surgical removal of breasts or ovaries.

Authorization of the 23andMe GHR tests was supported by data from peer-reviewed, scientific literature that demonstrated a link between specific genetic variants and each of the 10 health conditions. The published data originated from studies that compared genetic variants present in people with a specific condition to those without that condition. The FDA also reviewed studies, which demonstrated that 23andMe GHR tests correctly and consistently identified variants associated with the 10 indicated conditions or diseases from a saliva sample.

The FDA requires the results of all DTC tests used for medical purposes be communicated in a way that consumers can understand and use. A user study showed that the 23andMe GHR tests’ instructions and reports were easy to follow and understand. The study indicated that people using the tests understood more than 90 percent of the information presented in the reports.

Risks associated with use of the 23andMe GHR tests include false positive findings, which can occur when a person receives a result indicating incorrectly that he or she has a certain genetic variant, and false negative findings that can occur when a user receives a result indicating incorrectly that he or she does not have a certain genetic variant. Results obtained from the tests should not be used for diagnosis or to inform treatment decisions. Users should consult a health care professional with questions or concerns about results.

The FDA granted market authorization of the Personal Genome Service GHR tests to 23andMe, Inc.

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

Citation

https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm551185.htm

Copyright U.S. Food and Drug Administration

 

Genetic Assessment Developed to Determine Risk for Age-Associated Alzheimer’s Disease

(University of California San Diego Health Sciences) An international team of scientists, led by researchers at University of California San Diego School of Medicine and University of California San Francisco, has developed a novel genetic score that allows individuals to calculate their age-specific risk of developing Alzheimer’s disease (AD), based upon genetic information.

A description of the polygenic hazard scoring (PHS) system and its validation are published in the March 21 online issue of PLOS Medicine.

“We combined genetic data from large, independent cohorts of patients with AD with epidemiological estimates to create the scoring, then replicated our findings on an independent sample and validated them with known biomarkers of Alzheimer’s pathology,” said co-first author Rahul S. Desikan, MD, PhD, clinical instructor in the UCSF Department of Radiology & Biomedical Imaging.

Specifically, the researchers combined genotype-derived polygenic information with known AD incidence rates from the U.S. population to derive instantaneous risk estimates for developing AD.

“For any given individual, for a given age and genetic information, we can calculate your ‘personalized’ annualized risk for developing AD,” said Desikan.

“That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information. We think these measures of polygenetic risk, of involving multiple genes, will be very informative for early AD diagnosis, both in determining prognosis and as an enrichment strategy in clinical trials.”

To conduct the study, the research team analyzed genotype data from more than 70,000 AD patients and normal elderly controls who were participating in several projects, such as the Alzheimer’s Disease Genetics Consortium, the National Alzheimer’s Coordinating Center and the Alzheimer’s Disease Neuroimaging Initiative.

The team scrutinized the data for AD-associated single nucleotide polymorphisms (SNPs), which are variations of a single nucleotide or DNA building block that occur at a specific position in the genome. There is some SNP variation in genomic information in all humans, which affects individual susceptibility to disease. In this case, the researchers looked at SNPs linked to AD risk and for APOE status. Persons with the E4 variant in the APOE gene are known to be at greater risk of developing late-onset AD.

The researchers developed a continuous polygenic hazard score or PHS based upon this data to predict age-specific risk of developing AD, then tested it in two independent cohorts or defined groups of people. They found persons in the top PHS quartile developed AD at a considerably lower age and had the highest yearly AD incidence rate.

Importantly, PHS also identified people who were cognitively normal at baseline but eventually developed AD. Even among people who did not have the APOE E4 allele, the most important genetic risk factor for AD, PHS informed age of onset; individuals with high PHS scores developed AD 10-15 years earlier than individuals with low PHS.

The authors found that PHS strongly predicted empirical age of AD onset and progression from normal aging to AD, with strongly associated neuropathology and biomarkers of AD neurodegeneration.

“From a clinical perspective, the polygenic hazard score provides a novel way not just to assess an individual’s lifetime risk of developing AD, but also to predict the age of disease onset,” said senior author Anders Dale, PhD, director of the Center for Translational Imaging and Precision Medicine and professor in neurosciences, radiology, psychiatry and cognitive science at UC San Diego School of Medicine.

“Equally important, continuous polygenic testing of AD genetic risk can better inform prevention and therapeutic trials and be useful in determining which individuals are most likely to respond to therapy.”

The authors note several limitations to their study, beyond the need for broader and deeper validation studies. For example, their databases primarily represented individuals of European descent and thus are not indicative of AD incidence and genetic risk in other ethnicities, such as African-American or Latino.

“This limitation is an unfortunate product of available genetic studies. To have good predictive performance, the genetic risk score requires a large amount of data to train, but currently only European cohorts have reached this critical mass,” said co-first author Chun Chieh Fan, MD, in the Department of Cognitive Science at UC San Diego.

But “given the genome-wide association studies across ethnic populations that are emerging, the health disparities in the field of genetic prediction will be removed,” Fan added.

Citation

https://health.ucsd.edu/news/releases/Pages/2017-03-21-genetic-assessment-developed-to-determine-risk-for-age-related-alzheimers.aspx

By  Scott LaFee and Laura Kurtzman, UCSF

Journal Reference:

Rahul S. Desikan, Chun Chieh Fan, Yunpeng Wang, Andrew J. Schork, Howard J. Cabral, L. Adrienne Cupples, Wesley K. Thompson, Lilah Besser, Walter A. Kukull, Dominic Holland, Chi-Hua Chen, James B. Brewer, David S. Karow, Karolina Kauppi, Aree Witoelar, Celeste M. Karch, Luke W. Bonham, Jennifer S. Yokoyama, Howard J. Rosen, Bruce L. Miller, William P. Dillon, David M. Wilson, Christopher P. Hess, Margaret Pericak-Vance, Jonathan L. Haines, Lindsay A. Farrer, Richard Mayeux, John Hardy, Alison M. Goate, Bradley T. Hyman, Gerard D. Schellenberg, Linda K. McEvoy, Ole A. Andreassen, Anders M. Dale. Genetic assessment of age-associated Alzheimer disease risk: Development and validation of a polygenic hazard score. PLOS Medicine, 2017; 14 (3): e1002258 DOI: 10.1371/journal.pmed.1002258

Copyright © 2017 Regents of the University of California.

 

Cancer Drug That Might Slow Parkinson’s, Alzheimer’s Headed For Bigger Tests

(NPR.org) Scientists are hoping that a single drug can treat two devastating brain diseases: Parkinson’s and Alzheimer’s.

The drug is nilotinib, which is approved to treat a form of leukemia.

In late 2015, researchers at Georgetown University Medical Center found that small doses of the drug appeared to help a handful of people with Parkinson’s disease and a related form of dementia. They’d tried the unlikely treatment because they knew nilotinib triggered cells to get rid of faulty components — including the ones associated with several brain diseases.

A colored magnetic resonance imaging (MRI) scans of the brain of a 76-year-old patient with dementia shows the brain has atrophied and the dark brown fluid-filled spaces have become enlarged. Zephyr/Science Source

Results of that preliminary study generated a lot of excitement because there is currently no treatment that can slow or halt the brain damage caused by either Parkinson’s or Alzheimer’s.

“Our phones were basically (ringing) off the hook,” says Fernando Pagan, medical director of the translational neurotherapeutics program at Georgetown.

Many researchers were cautious, though.

“It was such a small trial, there was no placebo control and it really wasn’t designed to assess efficacy,” says J. Paul Taylor, chair of the cell and molecular biology department at St. Jude Children’s Research Hospital in Memphis.

So Georgetown is launching two larger and more rigorous trials of nilotinib, both designed with input from the Food and Drug Administration. One of the trials will enroll 75 patients with Parkinson’s disease, the other will enroll 42 patients with Alzheimer’s.

“This is going to help us identify what might have been a placebo effect and what is truly the effect of the medication,” Pagan says.

Nilotinib seems to work by eliminating toxic proteins that build up in the brains of people with Parkinson’s and Alzheimer’s. The drug activates a mechanism in brain cells that acts like a sort of garbage disposal, Pagan says.

“Our drug goes into the cells to turn on that garbage disposal mechanism,” Pagan says.

“And if we’re able to degrade these proteins, we could potentially stop the progression of this disorder.”

The primary goal of the studies is to learn whether this powerful cancer drug is safe enough for patients with brain diseases. But the new studies should also provide better evidence about whether the drug really works.

That possibility attracts patients like Jonathan Lessin, a former anesthesiologist in the Washington D.C. area. Lessin was diagnosed with Parkinson’s 14 years ago, when he was just 38.

Parkinson’s gradually kills off brain cells that control movement. And for a decade after his diagnosis, drugs and a treatment called deep brain stimulation allowed Lessin to continue working. He retired several years ago, when his symptoms progressed to the point that he feared he might not be able to provide first-rate care for his patients.

Since then, the disease has caused Lessin’s speech to become slightly slurred. “It’s slowly progressing,” he says. “My balance is getting worse and worse. I’m falling more and more during the day. But I’m still able to do things like rock climb and ski and bike.”

Lessin has been able to stay active thanks to treatments that help control symptoms. But the disease continues to eat away areas of his brain.

So Lessin was excited to learn about the Georgetown study, which held the tantalizing prospect of a drug that just might slow or halt that process.

“I’ve always been riding the leading edge of treatment,” Lessin says. “And I just figured I’d go for it.”

As a former physician, Lessin fully understands the limitations of the earlier trial, and the risks of taking a powerful cancer drug. But as someone with Parkinson’s, he sees an opportunity.

“I’m very optimistic,” he says. “I’ve seen it cure Parkinson’s in mice. I’ve seen people who can talk again, walk again, which is very encouraging.”

There’s good reason for patients with Parkinson’s, Alzheimer’s and other neurodegenerative diseases to be optimistic these days, Taylor says.

Drugs like nilotinib are coming along because years of research have provided a much better understanding of how these damage the brain, he says.

“Now we’re in the payoff phase.”

Taylor still isn’t sure whether nilotinib will live up to its early promise. But, he says,

“If the results of this trial don’t turn out to be as exciting as the very tiny trial suggested, I would not get too pessimistic because there are other developments that are in the wings.”

The Georgetown studies are enrolling patients now and will take more than a year to complete.

Information about the Parkinson’s study can be found here. Information about the Alzheimer’s study is available here.

Citation

http://www.npr.org/sections/health-shots/2017/03/15/520170960/cancer-drug-that-might-slow-parkinson-s-alzheimer-s-headed-for-bigger-tests

By Jon Hamilton

© 2017 npr

 

Alzheimer’s Death Toll Nearly Doubles in 15 Years

(WebMD) Alzheimer’s disease claims nearly twice as many American lives annually as it did just 15 years ago, a new report shows.

“And that’s frankly alarming,” said Keith Fargo, director of scientific programs and outreach at the Alzheimer’s Association, which produced the report.

“Now, a lot of people will think it’s because we’re living longer,” he added.

“And there is some truth to that. But there’s also an assumption that we should just expect to get Alzheimer’s disease as we get older. And that’s not true.

“Most people do not get Alzheimer’s, even if they live into their 80s or 90s. It’s not normal. It’s not something that we should accept. We’ve definitely got to do something about it,” Fargo said.

The report also found that more than 5 million American seniors aged 65 and older now live with the memory-robbing disease.

That represents approximately 10 percent of all the nation’s seniors, and that number is projected to jump to nearly 14 million by 2050. In fact, nearly half a million seniors are expected to develop the disease in 2017 alone.

Another 200,000 Americans under the age of 65 also struggle with the disease, the report found.

And those statistics come with a hefty price tag: It costs $259 billion a year for Alzheimer’s care. That amount is expected to reach $$1.1 trillion by 2050, the report estimated.

Dr. Anton Porsteinsson is director of the Alzheimer’s Disease Care, Research and Education Program at the University of Rochester School of Medicine in Rochester, N.Y. He said the rising numbers likely reflect a number of different factors in play.

“Partly, it is due to increasing numbers of older individuals, partly due to success in treating other leading causes of death, and partly due to increasing awareness that AD [Alzheimer’s] is a lethal disease,” Porsteinsson said.

Among the report’s additional findings: Alzheimer’s is now the fifth leading cause of death among seniors; the sixth leading cause of fatalities among all Americans; and the only disease among the nation’s top 10 biggest killers for which there is no prevention, no way to slow progression and no cure.

“And the costs are now completely out of control,” added Fargo, with the total annual cost for Alzheimer’s and dementia care in excess of a quarter trillion dollars.

Another highlighted concern: the “especially burdensome” ordeal Alzheimer’s caregivers experience while attending to the needs of loved ones as the patient suffers across-the-board mental and physical decline.

In 2016, more than 15 million Alzheimer’s caregivers provided just over 18 billion hours of unpaid care, valued at $230 billion.

And those caregivers suffer their own health consequences: More than a third (35 percent) report their health has worsened since assuming caregiver duties, compared with 19 percent of caregivers for older people without dementia. Depression and anxiety also plague dementia caregivers more often, the report found.

Still, the report was not entirely bleak, spotlighting growing efforts to identify telltale signs of developing disease.

The goal is to hone in on neurological signs — including changes in brain size, shifts in spinal fluid content, and/or the growth of nerve plaques in the brain — that could allow rapid detection of pre-symptomatic Alzheimer’s.

“It’s a window into the future,” Fargo said.

“If you ask where Alzheimer’s disease research is headed, that’s where it’s headed.”

“We believe that in the coming years we’ll have tests that you can do in the doctor’s office that will let you know your risk for Alzheimer’s,” he noted. And that, he suggested, “could open the door for prevention.”

Fargo noted that, even in the absence of effective treatments or a cure, early diagnosis would be a boon for research and would give patients a head start on planning for their future.

Yet, Porsteinsson suggested that the future of these telltale signs, known as biomarkers, remains unclear.

“Biomarkers are particularly important when it comes to research and development of future potential treatments,” he said.

On the other hand, he stressed that “the utility of biomarkers in current care is intensely debated.

“The biomarkers are expensive,” Porsteinsson noted.

“And it is a question how much a positive or negative finding will change approach to care.

“Having said that,” he added, “it often matters greatly to patients and their families to know exactly what they have and what to expect.”

Citation

http://www.webmd.com/alzheimers/news/20170307/annual-death-toll-from-alzheimers-nearly-doubles-in-15-years#1

SOURCES: Keith Fargo, Ph.D., director, scientific programs and outreach, Alzheimer’s Association, New York City; Anton Porsteinsson, M.D., professor, psychiatry, and director, Alzheimer’s Disease Care, Research and Education Program, University of Rochester School of Medicine, Rochester, N.Y.; March 7, 2017, 2017 Alzheimer’s Disease Facts and Figures

Copyright © 2013-2017 HealthDay. All rights reserved

 

Sugar’s “Tipping Point” Link to Alzheimer’s Disease Revealed

(University of Bath) For the first time a “tipping point” molecular link between the blood sugar glucose and Alzheimer’s disease has been established by scientists, who have shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer’s.

Abnormally high blood sugar levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer’s disease is less familiar.

Diabetes patients have an increased risk of developing Alzheimer’s disease compared to healthy individuals. In Alzheimer’s disease abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer’s was not understood.

But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King’s College London, have unraveled that link.

By studying brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation, the team discovered that in the early stages of Alzheimer’s glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer’s disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the ‘tipping point’ in disease progression. It appears that as Alzheimer’s progresses, glycation of these enzymes increases.

The study is published in the journal Scientific Reports.

Professor Jean van den Elsen, from the University of Bath Department of Biology and Biochemistry, said:

“We’ve shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer’s disease. We are now investigating if we can detect similar changes in blood.

“Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer’s to develop.

Dr Rob Williams, also from the Department of Biology and Biochemistry, added:

“Knowing this will be vital to developing a chronology of how Alzheimer’s progresses and we hope will help us identify those at risk of Alzheimer’s and lead to new treatments or ways to prevent the disease.

Dr Omar Kassaar, from the University of Bath, added:

“Excess sugar is well known to be bad for us when it comes to diabetes and obesity, but this potential link with Alzheimer’s disease is yet another reason that we should be controlling our sugar intake in our diets.”

Globally there are around 50 million people with Alzheimer’s disease, and this figure is predicted to rise to more than 125 million by 2050. The global social cost of the disease runs into the hundreds of billions of dollars as alongside medical care patients require social care because of the cognitive effects of the disease.

The study was funded by the Dunhill Medical Trust. Human brain tissue for this study was provided through Brains for Dementia Research, a joint initiative between Alzheimer’s Society and Alzheimer’s Research UK in association with the Medical Research Council.

Citation

http://www.bath.ac.uk/research/news/2017/02/23/sugar-alzheimer%E2%80%99s-disease/

Journal Reference:

Omar Kassaar, Marta Pereira Morais, Suying Xu, Emily L. Adam, Rosemary C. Chamberlain, Bryony Jenkins, Tony James, Paul T. Francis, Stephen Ward, Robert J. Williams, Jean van den Elsen. Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer’s Disease. Scientific Reports, 2017; 7: 42874 DOI: 10.1038/srep42874

© 2017 University of Bath

 

High Blood Pressure Onset in Late Life May Protect Against Dementia

(Alzheimer’s Association) New study results published online today in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggest that onset of high blood pressure later in life is associated with lower dementia risk after age 90, especially if hypertension is developed at age 80 or older.

High blood pressure and other heart health risk factors are generally thought to increase dementia risk. These new findings challenge this idea and add to scientists’ understanding of hypertension and dementia risk over a person’s life course.

Researchers at the University of California, Irvine and colleagues followed 559 people for an average of 2.8 years to investigate the relationship between dementia, age of hypertension onset, and blood pressure measurements. All participants are from an ongoing, long-term study of people age 90 and older known as The 90+ Study.

At enrollment, participants did not have dementia, were 93 years old on average, and 69 percent female. They received dementia assessments every six months during the study period. During the follow-up period, 224 (40%) of the participants were diagnosed with dementia.

The researchers found that study participants who reported hypertension onset at age 80 to 89 were 42 percent less likely to develop dementia after age 90 compared to those who reported no history of high blood pressure. Participants whose hypertension began at age 90 or older were at even lower risk–63 percent less likely to develop dementia. These associations were statistically significant and independent of whether participants were taking medications to treat hypertension.

“In this first-of-its-kind study, we find that hypertension is not a risk factor for dementia in people age 90 or over, but is actually associated with reduced dementia risk,” said first author Maria Corrada, M.S., Sc.D., Professor of Neurology and Epidemiology at the University of California, Irvine.

“This relationship had not yet been examined in groups of older people in their 80s or 90s, known as the ‘oldest old.'”

The authors also measured study participants’ blood pressure at enrollment. Those in the hypertensive range at baseline were at lower risk for dementia compared to those with blood pressure in the normal range. While these results were not statistically significant, the researchers observed that dementia risk declined as hypertension severity increased–a trend consistent with the idea that, in this age group, hypertension may protect the brain from insults that lead to dementia.

“These new findings suggest some risk factors for dementia may change over the course of our lives,” said Maria Carrillo, Ph.D., Alzheimer’s Association Chief Science Officer.

“We have seen similar results in past studies comparing body mass in older adults with dementia risk.”

A study published in January 2008 of 255 people aged 75 or older living in the Kungsholmen borough of Stockholm, Sweden, found those who were overweight had a lower dementia risk. A study published in March the following year of almost 3,000 adults near age 75 on average who were part of an observational study called the Cardiovascular Health Study had similar results: those who were underweight had an increased risk for dementia while those who were obese had a reduced risk.

“Before we can make the leap to suggesting changes to blood pressure recommendations for reducing dementia risk in clinical care, we need more research to confirm and explain our findings,” said Dr. Corrada.

“This includes investigations into the underlying biology of hypertension and brain function.”

The authors suggest several potential reasons for the association between hypertension and dementia risk observed in the study. These include that blood pressure may need to reach a certain level to maintain adequate blood flow in the brain for normal cognition, and that this level may change with age. Another explanation that the authors note is less likely, but possible, is that blood pressure drops before the onset of dementia as a consequence of brain cell deterioration, and thus older people who are not developing dementia will have higher blood pressure.

The authors acknowledge the study has several limitations, including that participants were mostly women and all were residents of a large retirement community in Orange County, California, and therefore not representative of the entire “oldest old” population.

“We need to understand the bigger picture of what protects brain health throughout our entire lives, including our later years,” said Dr. Carrillo.

“Looking at dementia in this group is critical since it is the fastest growing segment of the U.S. population with the highest rate of dementia.”

“Age of Onset of Hypertension and Risk of Dementia in the Oldest Old: The 90+ Study” is available to subscribers of Alzheimer’s & Dementia at http://www.alzheimersanddementia.com. Preliminary results of this study were first presented at the Alzheimer’s Association International Conference (AAIC) in July 2014 in Copenhagen, Denmark.

Citaition

https://www.eurekalert.org/pub_releases/2017-01/aa-sfh011117.php

Copyright © 2017 by the American Association for the Advancement of Science (AAAS)

 

Medicare Now Provides Coverage for Critical Alzheimer’s Care and Support Services

(Alzheimer’s Association) For the over five million American living with Alzheimer’s disease and their families, early detection and diagnosis is an important first step to managing their health. Currently, less than half of seniors diagnosed with dementia, or their caregivers, are aware of the diagnosis, even though Medicare covers the process for getting diagnosed.

Why is that? Studies show that one reason doctors don’t disclose the diagnosis of Alzheimer’s or a related dementia, is because of the insufficient time and resources to provide support to patients and caregivers at the time of diagnosis, including a discussion of treatment options and support services.

However, recent developments show promise in addressing this critical gap in care and support. Starting this month, Medicare will reimburse doctors for taking the time to test for dementia, document the diagnosis and discuss care planning with their patients.

Care planning and documentation of a diagnosis are crucial to improving outcomes and quality of care. Care planning allows people to learn about treatment options, enroll in clinical trials and access support services. Studies suggest that care planning can improve the long-term health of caregivers, as well.

Documentation ensures all health care providers know of the diagnosis and can more effectively coordinate care and properly manage other chronic conditions, medications and care transitions.

Among people with Alzheimer’s or a related dementia, over 85% have one or more other chronic conditions. Alzheimer’s complicates the management of these conditions, and thus increases cost. For example, care for a senior with diabetes and Alzheimer’s costs Medicare 81% more than the care for a senior who has diabetes but no Alzheimer’s.

The updates on Medicare coverage would help reduce cost by ensuring that critical steps are taken by health care providers to help families immediately after a diagnosis. This recent development is a result of the HOPE for Alzheimer’s Act (Health Outcomes, Planning and Education for Alzheimer’s Act S. 857 / H.R. 1559).

Specifically, under the Hope for Alzheimer’s Act, Medicare beneficiaries, who are newly diagnosed with Alzheimer’s disease, would receive coverage for comprehensive care planning services for themselves and their caregivers.

In an analysis by former Congressional Budget Office staff, this new legislation is estimated to reduce federal spending by $692 million over the next ten years. Savings would come from reduced hospitalizations and emergency room visits among seniors, and some savings resulting from better medication and other chronic condition management.

Alzheimer’s Association grassroots advocates and staff have held thousands of congressional meetings to secure support for the HOPE for Alzheimer’s Act since the bill’s introduction, and have worked tirelessly to secure support for the benefit at The Centers for Medicare & Medicaid Services (CMS). We will continue to engage CMS to ensure the service’s maximum impact for people living with the disease and their caregivers.

Alzheimer’s Association

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Citation

http://www.alzheimersblog.org/2017/01/10/ medicare-coverage-critical-alzheimers-care-support-services/

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