Evidence Supporting Three Interventions That Might Slow Cognitive Decline and the Onset of Dementia is Encouraging but Insufficient to Justify Public Health Campaign on Their Adoption

(National Academies of Sciences, Engineering, and Medicine) Cognitive training, blood pressure management for people with hypertension, and increased physical activity all show modest but inconclusive evidence that they can help prevent cognitive decline and dementia, but there is insufficient evidence to support a public health campaign encouraging their adoption, says a new report from the National Academies of Sciences, Engineering, and Medicine.  Additional research is needed to further understand and gain confidence in their effectiveness, said the committee that conducted the study and wrote the report.

“There is good cause for hope that in the next several years much more will be known about how to prevent cognitive decline and dementia, as more clinical trial results become available and more evidence emerges,” said Alan I. Leshner, chair of the committee and CEO emeritus, American Association for the Advancement of Science.

“Even though clinical trials have not conclusively supported the three interventions discussed in our report, the evidence is strong enough to suggest the public should at least have access to these results to help inform their decisions about how they can invest their time and resources to maintain brain health with aging.”

An earlier systematic review published in 2010 by the Agency for Healthcare Research and Quality (AHRQ) and an associated “state of the science” conference at the National Institutes of Health had concluded that there was insufficient evidence to make recommendations about any interventions to prevent cognitive decline and dementia.

Since then, understanding of the pathological processes that result in dementia has advanced significantly, and a number of clinical trials of potential preventive interventions have been completed and published.  In 2015, the National Institute on Aging (NIA) contracted with AHRQ to conduct another systematic review of the current evidence.  NIA also asked the National Academies to convene an expert committee to help inform the design of the AHRQ review and then use the results to make recommendations to inform the development of public health messaging, as well as recommendations for future research.

This report examines the most recent evidence on steps that can be taken to prevent, slow, or delay the onset of mild cognitive impairment and clinical Alzheimer’s-type dementia as well as steps that can delay or slow age-related cognitive decline.

Overall, the committee determined that despite an array of advances in understanding cognitive decline and dementia, the available evidence on interventions derived from randomized controlled trials – considered the gold standard of evidence – remains relatively limited and has significant shortcomings.

Based on the totality of available evidence, however, the committee concluded that three classes of interventions can be described as supported by encouraging but inconclusive evidence.  These interventions are:

  • cognitive training – which includes programs aimed at enhancing reasoning and problem solving, memory, and speed of processing – to delay or slow age-related cognitive decline.  Such structured training exercises may or may not be computer-based.
  • blood pressure management for people with hypertension – to prevent, delay, or slow clinical Alzheimer’s-type dementia.
  • increased physical activity – to delay or slow age-related cognitive decline.

Cognitive training has been the object of considerable interest and debate in both the academic and commercial sectors, particularly within the last 15 years.  Good evidence shows that cognitive training can improve performance on a trained task, at least in the short term.  However, debate has centered on evidence for long-term benefits and whether training in one domain, such as processing speed, yields benefits in others, such as in memory and reasoning, and if this can translate to maintaining independence in instrumental activities of daily living, such as driving and remembering to take medications.

Evidence from one randomized controlled trial suggests that cognitive training delivered over time and in an interactive context can improve long-term cognitive function as well as help maintain independence in instrumental activities of daily living for adults with normal cognition.  However, results from other randomized controlled trials that tested cognitive training were mixed.

Managing blood pressure for people with hypertension, particularly during midlife – generally ages 35 to 65 years – is supported by encouraging but inconclusive evidence for preventing, delaying, and slowing clinical Alzheimer’s-type dementia, the committee said.

The available evidence, together with the strong evidence for blood pressure management in preventing stroke and cardiovascular disease and the relative benefit/risk ratio of antihypertensive medications and lifestyle interventions, is sufficient to justify communication with the public regarding the use of blood pressure management, particularly during midlife, for preventing, delaying, and slowing clinical Alzheimer’s-type dementia, the report says.

It is well-documented that physical activity has many health benefits, and some of these benefits – such as stroke prevention – are causally related to brain health.  The AHRQ systematic review found that the pattern of randomized controlled trials results across different types of physical activity interventions provides an indication of the effectiveness of increased physical activity in delaying or slowing age-related cognitive decline, although these results were not consistently positive.

However, several other considerations led the committee to conclude that the evidence is sufficient to justify communicating to the public that increased physical activity for delaying or slowing age-related cognitive decline is supported by encouraging but inconclusive evidence.

None of the interventions evaluated in the AHRQ systematic review met the criteria for being supported by high-strength evidence, based on the quality of randomized controlled trials and the lack of consistently positive results across independent studies.  This limitation suggests the need for additional research as well as methodological improvements in the future research.

The National Institutes of Health and other interested organizations should support further research to strengthen the evidence base on cognitive training, blood pressure management, and increased physical activity, the committee said.  Examples of research priorities for these three classes of interventions include evaluating the comparative effectiveness of different forms of cognitive training interventions; determining whether there are optimal blood pressure targets and approaches across different age ranges; and comparing the effects of different forms of physical activity.

When funding research on preventing cognitive decline and dementia, the National Institutes of Health and other interested organizations should identify individuals who are at higher risk of cognitive decline and dementia; increase participation of underrepresented populations; begin more interventions at younger ages and have longer follow-up periods; use consistent cognitive outcome measures across trials to enable pooling; integrate robust cognitive outcome measures into trials with other primary purposes; include biomarkers as intermediate outcomes; and conduct large trials designed to test the effectiveness of an intervention in broad, routine clinical practices or community settings.

The study was sponsored by the National Institute on Aging.  The National Academies of Sciences, Engineering, and Medicine are private, nonprofit institutions that provide independent, objective analysis and advice to the nation to solve complex problems and inform public policy decisions related to science, technology, and medicine.  The National Academies operate under an 1863 congressional charter to the National Academy of Sciences, signed by President Lincoln.  For more information, visit http://national-academies.org.



Copyright © 2017 National Academy of Sciences. All rights reserved.


US Death Rates from Alzheimer’s Disease Increased 55 Percent from 1999 to 2014

(MedicalNewsToday) Death rates from Alzheimer’s disease (AD) increased 55 percent between 1999 and 2014, according to data released today in the CDC’s Morbidity and Mortality Weekly Report. The number of Alzheimer’s deaths at home also increased during the same period, from 14 percent to 25 percent, suggesting an increase in the number of caregivers that would benefit from support, including education and case management services.

Alzheimer’s disease is a fatal form of dementia. It is the sixth leading cause of death in the United States, accounting for 3.6 percent of all deaths in 2014. It is the fifth leading cause of death among people ages 65 years and older in the United States.

“Millions of Americans and their family members are profoundly affected by Alzheimer’s disease,” said CDC Acting Director Anne Schuchat, M.D.

“Our new study reveals an increase in the incidence of Alzheimer’s disease-related deaths. As the number of older Americans with Alzheimer’s disease rises, more family members are taking on the emotionally and physically challenging role of caregiver than ever before. These families need and deserve our support.”

This study is the first to provide county-level rates for deaths caused by AD. CDC researchers analyzed state- and county-level death certificate data from the National Vital Statistics System to identify deaths with AD reported as the underlying cause.

According to the analysis, possible reasons for the increase include the growing population of older adults in the U.S., increases in diagnosis of AD at earlier stages, increased reporting by physicians and others who record the cause of death, and fewer deaths from other causes of deaths for the elderly, such as heart disease and stroke.

Key findings from analysis of AD rates

  • The death rate increased 55 percent – from 16.5 per 100,000 people in 1999 to 25.4 per 100,000 in 2014 after accounting for age.
  • Most Alzheimer’s deaths still occur in a nursing home or long-term care facility, but fewer in 2014 (54 percent) than in 1999 (68 percent).
  • Counties with the highest death rates were primarily in the Southeast; other areas with high rates included the Midwest and West Coast.

Age is the greatest risk factor for AD; most adults with the disease are 65 years or older. As fewer people die from other diseases, more survive into older adulthood and the risk for AD increases.

“As Alzheimer’s disease progresses, caregiving becomes very important. Caregivers and patients can benefit from programs that include education about Alzheimer’s disease, how to take care of themselves and their loved one, and case management to lessen the burden of care,” said Christopher Taylor, Ph.D., lead author and epidemiologist, Division of Population Health, CDC’s National Center for Chronic Disease Prevention and Health Promotion.

“Supportive interventions can lessen the burden for caregivers and improve the quality of care for people with Alzheimer’s disease.”

While there is currently no cure for AD, people should see a doctor if they experience symptoms affecting their daily life such as memory loss, difficulties with problem solving, or misplacing objects. Early diagnosis is important to allow patients and their families to begin planning medical and caregiving needs at all stages of the disease.

Article: Deaths from Alzheimer’s Disease – United States, 1999-2014, Christopher A. Taylor, PhD et al., Morbidity and Mortality Weekly Report, doi: 10.15585/mmwr.mm6620a1, published 26 May 2017.



Healthline Media UK Ltd, Brighton, UK.

© 2004-2017 All rights reserved.


Chronic Pain Linked to Increased Risk of Dementia in Older Adults

(UC San Francisco) Researchers at UC San Francisco have found that older people with persistent pain show quicker declines in memory as they age and are more likely to have dementia years later, an indication that chronic pain could somehow be related to changes in the brain that contribute to dementia.

The study, published in JAMA Internal Medicine, appears to be the first to make this association.

The researchers analyzed data from 10,000 participants aged 60 and up over a 12-year period. Those participants who said they were persistently troubled by moderate or severe pain in both 1998 and 2000 declined 9.2 percent faster in tests of memory function over the next 10 years than those who said they were not troubled by pain. The patients who complained about persistent pain also had a small but significantly increased likelihood of developing dementia overall.

Researchers found that the additional amount of memory decline in those who reported persistent pain suggested that these patients would likely have had a harder time with tasks of daily living, such as independently managing their medications and finances.

Elizabeth Whitlock, MD, MSc, a postdoctoral fellow in the UCSF Department of Anesthesia and Perioperative Care and the first author of the study, said the findings point toward new ways of thinking about how to protect older people from the cognitive insults of aging.

“Elderly people need to maintain their cognition to stay independent,” she said.

“Up to one in three older people suffer from chronic pain, so understanding the relationship between pain and cognitive decline is an important first step toward finding ways to help this population.”

The research, conducted in collaboration with members of UCSF’s Division of Geriatrics, suggests three potentially overlapping reasons for the association between chronic pain and dementia. An increased dementia risk could be caused by painkillers, such as opioids, which people are taking in greater numbers. It could also be that the experience of pain somehow compromises the brain’s ability to encode memories and other cognitive functions. Finally, it could be due to some other factor that was not measured in the study, and therefore could not be analyzed.

But even if this is the case, Whitlock said, the findings remain clinically relevant, because pain could be used as a marker for increased risk of future cognitive decline even if the biological basis of the association is still unclear.

The data that the researchers analyzed – an ongoing national study of older Americans called the Health and Retirement Study – did not include information about opioid use, so they could not tell which of their participants were taking the drugs.

While opioid use could be the cause of the cognitive changes they observed, Whitlock said, so could the pain itself. For example, a recent study of chronic pain sufferers found that those who took nonsteroidal anti-inflammatory drugs, such as ibuprofen, had nearly the same increased dementia risk as those taking opioids.

“This means we have to consider the potential direct effects of chronic pain on cognition,” she said.

People who suffer from chronic pain tend to have diminished attentional capacity and impaired memory, and Whitlock said that particularly when pain is severe or causes patients to ruminate, it could divert enough attention to interfere with the consolidation of memory.

Another possibility, she said, is that the emotional stress of being in pain activates stress-hormone pathways in the body that have been implicated in cognitive decline. If either is the case, she said, then effectively treating the pain could protect cognition.

Doctors often struggle to manage their patients’ pain, since current therapies, in addition to being addictive, do not always work. But Whitlock said that even those patients who continue to suffer, and may be experiencing a more rapid cognitive decline as a result, can still be helped with assistive devices, physical and occupational therapy, or strategies, such as mindfulness techniques, that are aimed at increasing self-efficacy and curbing the emotional impact of chronic pain.

“This is something I really feel we can do something about as clinicians,” Whitlock said. “It’s part of taking care of the whole patient.”



Article: Association Between Persistent Pain and Memory Decline and Dementia in a Longitudinal Cohort of Elders, Elizabeth L. Whitlock, MD, MSc et al., JAMA Internal Medicine, doi: 10.1001/jamainternmed.2017.1622, published online 5 June 2017.

Healthline Media UK Ltd, Brighton, UK.

© 2004-2017 All rights reserved.


U.S. Death Rate from Alzheimer’s Rose Dramatically Over 15 Years. Why?

(Washington Post) The Centers for Disease Control and Prevention has just put out a grim report about Alzheimer’s disease in the United States.

Death rates from Alzheimer’s climbed 55 percent from 1999 to 2014, CDC found, and the number of Americans afflicted is likely to rise rapidly in the coming years. About 5.5 million people 65 years and older have the disease — a wretched and fatal form of dementia that erases memories and ultimately can destroy mental and physical capacity. By 2050, that’s expected to more than double to 13.8 million people.

The report is based on state- and county-level death certificate data from the National Vital Statistics System, and CDC researchers said the sharp increase in death rates may be due to the aging population, earlier diagnosis and greater reporting by physicians.

There’s also the cruel fact that as we have become more sophisticated in our ability to operate and medicate away physical issues associated with aging — such as heart disease and stroke — there’s more time for something to go awry with our minds.

The new data, released in the Morbidity and Mortality Weekly Report, shows some disturbing racial and ethnic disparities. The increase in death rates from Alzheimer’s for African Americans was 99 percent; for Hispanics, 107 percent; and for Asian/Pacific Islanders, 151 percent. By comparison, the rate increase for whites was 54 percent.

George Vradenburg, the former AOL Time Warner senior executive who co-founded UsAgainstAlzheimer’s with his late wife Trish, has long lobbied for a bigger commitment by government, industry and scientists to find a cure.

“The CDC findings raise needed public awareness of how fast this disease is growing and destroying families, and how we must stand firm against any action that reduces the nation’s ability to innovate and speed cures,” he said in a statement Thursday.

Another important change identified by the report is where those with Alzheimer’s pass away. Though just over half still died in a nursing home or long-term-care facility in 2014, that percentage, as well as the percentage who died in a medical facility, was down significantly from 1999. During the same period, the proportion of people with the disease who died at home went from 13.9 percent to 24.9 percent. This is a key finding from a public health standpoint because of the impact on families.

“The debilitating nature of Alzheimer’s means that there are financial and societal costs borne by patients and their families, and by states and counties that operate publicly funded long-term care facilities,”

the researchers wrote. According to the Alzheimer’s Association, the disease and other dementias will cost the country $259 billion in health and care costs this year, with more than two-thirds covered by Medicare and Medicaid.

The researchers took the opportunity to recognize the toll the disease takes, not only on patients but on their loved ones. They called for more support for caregivers.

“Given the increasing number of Alzheimer’s deaths and persons with Alzheimer’s dying at home, there is a growing number of caregivers who likely can benefit from interventions like education, respite care, and home health assistance,” they wrote, adding that “such interventions can lessen the burden of care-giving and can improve the care received by persons with Alzheimer’s.”



Copyright The Washington Post


Probe of Alzheimer’s Follows Paths of Infection

(Harvard University) Starting with microbes, Harvard-MGH researchers outline a devastating chain of events.

What if the bad-boy protein of Alzheimer’s disease — amyloid beta — isn’t so bad after all?

Harvard researchers found themselves asking that question several years ago after noticing remarkable similarities between amyloid beta, thought to be a major player in the disease’s progression, and proteins active in the body’s immune system.

That discovery has blossomed into a new avenue of investigation against the nation’s leading cause of dementia, sixth-deadliest illness, and — according to a 2011 survey — the runner-up to cancer in health fears among the public.

Led by Robert Moir, an assistant professor in neurology at Harvard Medical School (HMS) and Massachusetts General Hospital (MGH), and Rudolph Tanzi, Joseph P. and Rose F. Kennedy Professor of Child Neurology and Mental Retardation at HMS and MGH, the work is focused on whether the development of amyloid beta plaques in the brain — a hallmark of Alzheimer’s disease and the target of several recent drug candidates — might in many cases be a response to infection.

Proven correct, the explanation would fill a significant blank in our framework for the causes of Alzheimer’s disease, create a new understanding of amyloid beta’s role in the body, and possibly open new fronts for treating or preventing the condition by attacking infection before plaques begin to form.

It also has the potential to lump Alzheimer’s with diabetes and other autoimmune diseases in which a revved-up immune system goes too far and turns on the body. Scientists have already noted enough similarities between Alzheimer’s and diabetes that some have wondered whether Alzheimer’s should be thought of as “type 3 diabetes.”

Though knowledge about Alzheimer’s has advanced in recent decades, its causes are only partially understood. In the late 1980s and early 1990s, Tanzi played a role in discovering a trio of genes that cause early onset Alzheimer’s, which runs in a small number of families and can strike before age 50. That condition, also called familial Alzheimer’s, accounts for only about 5 percent of cases.

The remaining cases, called sporadic Alzheimer’s, typically occur later in life, in a person’s mid-60s or beyond. Advancing age is the biggest risk factor — scientists don’t know exactly why — and genetics also plays a role, though less so than in early onset Alzheimer’s.

A variant of the gene APOE, or alipoprotein E, has been identified as a risk factor in sporadic Alzheimer’s. But having the variant doesn’t make the disease inevitable, and not having it doesn’t rule it out. Which has left scientists wondering what other non-genetic factors are at play.

A significant roadblock to discovery has been a lack of clarity on the role of amyloid beta in the body. The Alzheimer’s community has largely viewed it as an aberrant byproduct that serves no useful purpose in the brain — “metabolic garbage,” as Tanzi once put it.

That view has persisted even as understanding of other aspects of Alzheimer’s has advanced. The prevailing hypothesis today is that amyloid beta aggregates to form plaques in the brain. Those plaques then cause the development of tangles made up of the protein tau within nerve cells. This triggers inflammation — a natural immune response that in this case compounds the damage. Connections between nerve cells are severed and the cells die. Cognitive ability inexorably declines, producing the disease’s most feared outcome.

The idea that Alzheimer’s disease might be caused by infection isn’t new, Moir noted. In fact, in the 1970s and 1980s, some scientists considered it the strongest hypothesis. That changed in 1984 with the discovery of amyloid beta, which came to dominate subsequent research.

Though support for what came to be called the “pathogen hypothesis” has endured, Tanzi, director of MGH’s Genetics and Aging Research Unit, said that the disease outline he and Moir are developing differs in important ways. While the pathogen hypothesis is most often offered as an alternative to the amyloid beta hypothesis, Moir and Tanzi’s model is not an alternative, but rather fits within the amyloid beta-tau-inflammation paradigm. It fills in blanks, offering an explanation for how the process starts and for the true nature of amyloid beta.

Circumstantial evidence for the importance of amyloid beta is significant, Moir said. It appears to have developed some 400 million years ago and has not only survived evolutionary pressures to appear in humans today, but is present in 60 percent of vertebrates, including fish, reptiles, and birds.

Further, when Moir started to look more closely at the protein, he noticed similarities to key infection-fighting proteins called antimicrobial peptides in the innate immune system — the body’s first and most ancient line of defense.

“It tells you, first, it’s doing something important,” Moir said. “When we started to look at amyloid beta we realized this thing looked similar to antimicrobial peptides.”

Moir compared amyloid beta with LL-37, a potent part of the immune arsenal without which we’d all die from raging infections before reaching our terrible twos. That investigation, supported by a grant from the Cure Alzheimer’s Fund, led to a 2010 paper in which Moir’s team proposed that amyloid beta was an antimicrobial peptide, one that demonstrated infection-fighting abilities comparable to, and in some cases better than, penicillin.

A paper published last year in Science Translational Medicine took the work further, showing that amyloid beta protected against fungal and bacterial infection in nematode worms, laboratory mice, and cell cultures of human neuronal tissue. The work also showed that infecting the brains of lab mice with salmonella resulted in plaque formation 48 hours later, and that those mice lived longer than mice that didn’t develop the plaques.

When the researchers looked even closer, Moir said, at the center of each plaque was a single microbe.

Those findings, backed by the National Institutes of Health, the Cure Alzheimer’s Fund, and the Helmsley Charitable Trust, suggest a model of Alzheimer’s disease initiation that takes into account both infectious and genetic causes, Tanzi said. The process begins with amyloid beta plaques in the brain. In the case of an infection, the culprit is a single microbe — a virus, bacterium, or fungal spore. In the case of genetic disease, seeding relies on a higher-than-normal proportion of extra-long amyloid beta proteins. Amyloid beta, Tanzi explained, comes in two predominant forms. One is a chain of 40 amino acids, which tends to remain in solution, and the other 42 amino acids, which is the predominant form in plaques.

Tanzi compared the plaque formation — whether through amyloid beta’s 42 amino acid form or due to a microbe — to lighting a match. That leads to the development of tau protein tangles in nerve cells, which Tanzi compared to a brush fire. Then comes inflammation, a raging forest fire which Tanzi believes does much of the damage that leads to cognitive decline.

“It’s inflammation that really throws you down the slippery slope,” he said.

The brain was once thought of as kept relatively sterile by the blood-brain barrier, a membrane that selectively admits key molecules such as glucose and amino acids while blocking potentially harmful invaders.

Some notable diseases have long been known to slip through, including syphilis and rabies. But recently it’s become apparent that there’s a lot more life in there than scientists had understood, Moir said.

“The things creeping around in the brain will scare the heebie-jeebies out of you.”

Figuring out what is and isn’t in the brains of Alzheimer’s patients is the logical next step, one that Moir and Tanzi are undertaking through the Brain Microbiome Project. The researchers are examining brain bank samples from people who died of Alzheimer’s with those who didn’t. In the initial phase, they are searching for viruses by scanning for their genetic material.

When all is said and done, Moir said, it might be that Alzheimer’s is a “dysbiosis” of the brain, a sign that the microbiome is out of whack. Further, Tanzi said, if microbial culprits are identified, it might be possible to treat those infections early in life — possibly even with a vaccine — before the earliest plaques begin to form.

“What you see is a lot of stuff,” Moir said. “A lot of scary stuff.”


http://news.harvard.edu/gazette/story/2017/05/ devastating-chain-of-events-found-in-alzheimers-path/

By Alvin Powell, Harvard Staff Writer

© 2017 The President and Fellows of Harvard College


In-Home Care of Dementia Patients Falls Mainly on Women

(Stanford University School of Medicine) As the population ages, a surge in patients with dementia will place an inordinate burden on working women, risking “hard-fought gains for equality in the workplace,” according to Stanford researchers.

The responsibility of providing care to the vast number of patients with dementia expected over the next 20 years will disproportionately fall on working women, according to researchers at the Stanford University School of Medicine.

“The best long-term care insurance in our country is a conscientious daughter,” the authors wrote in a perspective piece published May 8 in JAMA Neurology.

The article points to a lack of affordable in-home care options in the United States other than unpaid family members, primarily women.

As more baby boomers reach retirement age, experts predict a corresponding surge in cases of dementia: By 2030, an estimated 8.4 million Americans are expected to be suffering from some form of the disease.

By 2030, it is estimated that 8.4 million Americans will have some form of dementia. Stanford researchers say that currently the responsibility of caring for people with dementia falls largely on female relatives.
Ocskay Bence/Shutterstock

Today, most of the care for these patients — 83 percent — is provided by unpaid family members, two-thirds of whom are women, the authors wrote.

“Wives are more likely to care for husbands than vice versa, and daughters are 28 percent more likely to care for a parent than sons,” the authors wrote, adding that because women now make up almost 50 percent of the workforce, these burgeoning demands will disproportionately fall on them — and put them at higher risk for lowering or exiting their career trajectory.

“Hard-fought gains toward equality in the workplace are at risk,” they wrote.

Health Care dilemma

Concern about this troubling health care dilemma grew out of research by a team of design fellows at Stanford’s Clinical Excellence Research Center. They were investigating ways to provide better care at lower costs for patients with dementia and other cognitive disorders.

“As our CERC fellows dug below the surface of dementia care, they detected a growing threat to health equity and tangible opportunities for action by policymakers and clinicians,” said co-author Arnold Milstein, MD, professor of medicine and director of CERC.

“I have a very personal history with this topic,” said Clifford Sheckter, MD, a CERC fellow and co-author of the article.

“My grandmother, my mom’s mom, got dementia when I was in college at UCLA. I remember my mom having to leave work two to three times a day to come home — whether my grandma had taken a fall or was calling my mom on the phone and screaming, it was relentless. It was so hard on my mom.”

The authors noted that while caregiving for loved ones with dementia can certainly be meaningful, the amount of time required — an average of 171 hours per month, according to the article — combined with the unpredictability of the job’s demands and unrelenting tasks, such as toileting and bathing, can be overwhelming. The article also asserts that “it’s not likely that men will step up and share in the caregiving anytime soon.”

If nothing is done to plan for this shift in caregiving demands, not only will women and their families suffer, an increase in costs will fall on employers from absenteeism, productivity loss, stress-related disability claims and health benefits plan spending, the article said.

“I come in contact with these patients often,” said co-author Nicholas Bott, PsyD, a neuropsychologist and CERC fellow.

“When you’re working with a patient who has this disease, you are also working with the family. It raises tensions for the entire family unit. It causes friction in the relationships. You end up doing a lot of triage for the family members.”

Raising Awareness

The article was written to sensitize physicians to the demands on family members caring for patients with dementia, the need to educate families about what will be required and the importance of referring them to caregiver support service, Milstein said.

“We hope to help clinicians see what kind of change in policy their advocacy might enable,” he said.

The authors also pointed to the role that employers could play in alleviating the strain of caregiving demands by adopting family-leave policies similar to Deloitte LLP, an international accounting and consulting firm that in August began offering employees up to 16 fully paid weeks to care for a family member, including aging family members.

“A six-week paid leave provided by employers, similar to family leave for new parents, would help caregivers to adjust to the new situation,” Bott said.

Federal tax subsidies allowing corporations to deduct the period of paid family leave may further help incentivize employers, the authors wrote.

Sheckter said with more support — from physicians, social services and particularly his mother’s employer — perhaps his grandmother could have continued to live at home. But eventually, overwhelmed by caregiving and work demands, his mother was forced to put his grandmother into a long-term care home, where she passed away.

“It’s kind of sad, but in our country we don’t do anything about caregiving for patients with dementia,” he said.



By Tracie White

©2017 Stanford Medicine


Stroke Prevention May Also Reduce Dementia

(University of Western Ontario) Ontario’s stroke prevention strategy appears to be having an unexpected, beneficial side effect: a reduction also in the incidence of dementia among older seniors.

A new paper by researchers at Western University, Lawson Health Research Institute and the Institute for Clinical Evaluative Sciences (ICES) shows there’s been a decade-long drop in new diagnoses of both stroke and dementia in the most at-risk group ­­—  those who are 80 or older.

“Some have said we’re on the cusp of an epidemic of dementia as the population ages,” said study author Joshua Cerasuolo, a PhD candidate in epidemiology and biostatistics at Western’s Schulich School of Medicine and Dentistry.

“What this data suggests is that by successfully fighting off the risks of stroke – with a healthy diet, exercise, a tobacco-free life and high blood-pressure medication where needed – we can also curtail the incidence of some dementias.

“The take-home message is that we can prevent some dementias by preventing stroke,” Cerasuolo said.

Published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, this is the first study that has looked at the demographics of both stroke and dementia across Ontario since the province pioneered Canada’s first stroke prevention strategy in 2000. That strategy includes more health centres able to manage stroke, more community and physician supports, better use of hypertensive mediation and well-promoted lifestyle changes to reduce risks. Five provinces have stroke strategies and five do not.

“With lifestyle changes, we can reduce our risks of both stroke and some dementias. That’s a pretty powerful one-two punch,” said Dr. Vladimir Hachinski, a clinical neuroscientist at Western’s Schulich School of Medicine and Dentistry, a Lawson Health Research Institute scientist and neurologist at London Health Sciences Centre. He is a world pioneer in stroke research and a co-supervisor of the research paper.

Hachinski said more research needs to take place to understand the specific relationships between stroke and dementia but this work suggests there are policy implications where stroke and dementia work can intersect.

“We have systems in place for stroke prevention and our hypothesis is that any studies looking at stroke prevention should also investigate dementia prevention,” Hachinski said.

“It’s a good-news story for Ontario and it could be a good-news story elsewhere.”

Most strokes are caused by the restriction or constriction of blood flow to the brain. Vascular dementia also develops as blood supply to the brain is reduced.

Hachinski said someone who has had a stroke is twice as likely to develop dementia. Someone who has had a diagnosis of stroke has also likely had several prior “silent” strokes that may have affected a patient’s cognitive abilities.

The data mining took place using information from ICES, based in Toronto.

Specifically, it shows that the incidence of new stroke diagnosis among highest-risk group, people aged 80-plus, dropped by 37.9 per cent in a span of a little more than a decade. During the same timeframe, the incidence of dementia diagnoses in that age group fell by 15.4 per cent.

“As clinicians and researchers, we are still trying to get a handle on how to reduce a person’s chances of dementia late in life. Some we can’t influence – yet – but here is a pretty clear indication that we can take specific definitive steps to reduce our chances of dementia related to vascular disease,” Hachinski said.

Video of the research can be found here:

The journal is making the article, “Population-based stroke and dementia incidence trends: Age and sex variations,” available free online in advance of publication as an “article in press, corrected proof” until May 30.


  • Data from 5.5 million Ontarians was analyzed to calculate stroke and dementia incidence rates from 2002 to 2013 in the first population-based demographics study of both.
  • Researchers discovered stroke incidence during those 12 years decreased across the board for people older than 50. For people aged 80-plus, stroke incidence fell by 37.9% while dementia diagnoses decreased by 15.4%.
  • The decline in stroke and dementia incidence rates may mean successful stroke prevention has targeted shared risk factors of both conditions, especially in the older-age, highest-risk demographic.
  • The findings support an integrated system of stroke and dementia prevention measures.
  • Stroke-prevention measures include lifestyle changes (not smoking, healthy diet, exercise), using hypertensive medications as prescribed, access to appropriate health care.

http://mediarelations.uwo.ca/2017/05/01/ stroke-prevention-among-older-ontarians-may-also-reduce-risk-dementias/

© 1878 – 2017 Western University

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.



By Tim Newman

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