Midlife Cardiovascular Risk Factors May Increase Chances of Dementia

(NIH/National Institute of Neurological Disorders and Stroke) A large, long-term study suggests that middle aged Americans who have vascular health risk factors, including diabetes, high blood pressure and smoking, have a greater chance of suffering from dementia later in life. The study, published in JAMA Neurology, was funded by the National Institutes of Health (NIH).

“With an aging population, dementia is becoming a greater health concern. This study supports the importance of controlling vascular risk factors like high blood pressure early in life in an effort to prevent dementia as we age,” said Walter J. Koroshetz, M.D., director of NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which partially funded the study and created the Mind Your Risks® public health campaign to make people more aware of the link between cardiovascular and brain health.

“What’s good for the heart is good for the brain,” he added.

The study was led by Rebecca Gottesman, M.D., Ph.D., professor of neurology at Johns Hopkins University in Baltimore. Her team analyzed the data of 15,744 people who participated in the Atherosclerosis Risk in Communities (ARIC) study, funded by the NIH’s National Heart, Lung, and Blood Institute (NHLBI). From 1987-1989, the participants, who were black or white and 45-64 years of age, underwent a battery of medical tests during their initial examinations at one of four centers in four different states. Over the next 25 years they were examined four more times. Cognitive tests of memory and thinking were administered during all but the first and third exams.

Her team found that 1,516 participants were diagnosed with dementia during an average of 23 follow-up years. Initially, when they analyzed the influence of factors recorded during the first exams, the researchers found that the chances of dementia increased most strongly with age followed by the presence of APOE4, a gene associated with Alzheimer’s disease. Whites with one copy of the APOE4 gene had a greater chance of dementia than blacks. Other factors included race and education: blacks had higher chance of dementia than whites; those who did not graduate from high school were also at higher risk.

In agreement with previous studies, an analysis of vascular risk factors showed that participants who had diabetes or high blood pressure, also called hypertension, had a higher chance of developing dementia. In fact, diabetes was almost as strong a predictor of dementia as the presence of the APOE4 gene.

Unlike other studies, the researchers discovered a link between dementia and prehypertension, a condition in which blood pressure levels are higher than normal but lower than hypertension. Also, race did not influence the association between dementia and the vascular risk factors they identified. Diabetes, hypertension and prehypertension increased the chances of dementia for white and black participants. Finally, smoking cigarettes exclusively increased the chances of dementia for whites but not blacks.

“Our results contribute to a growing body of evidence linking midlife vascular health to dementia,” said Dr. Gottesman.

“These are modifiable risk factors. Our hope is that by addressing these types of factors early, people can reduce the chances that they will suffer from dementia later in life.”

Further analysis strengthened the idea that the vascular risk factors identified in this study were linked to dementia. For instance, in order to answer the question of whether having a stroke, which is also associated with the presence of vascular risk factors, may explain these findings, the team reanalyzed the data of participants who did not have a stroke and found similar results. Diabetes, hypertension, prehypertension and smoking increased the risk of dementia for both stroke-free participants and those who had a stroke.

Recently, in a separate study partially funded by the NIH’s National Institute on Aging, Dr. Gottesman’s team analyzed brain scans from a subgroup of ARIC participants who did not have dementia when they entered the study. They found that the presence of one or more vascular risk factors during midlife was associated with higher levels of beta amyloid, a protein that often accumulates in the brains of Alzheimer’s patients. This relationship was not affected by the presence of the APOE4 gene and not seen for risk factors present in later life. The presence of vascular risk factors detected in participants older than 65 years of age during the final examination was not associated with greater levels of beta amyloid.

“With many years of data from a large and diverse population, the ARIC study is a powerful source of information for medical research,” said Jacqueline D. Wright, Dr.P.H., program director at NHLBI.

“This epidemiologic study aimed to improve our understanding of atherosclerosis and heart disease and, through the investigators’ efforts; it has become a great resource for research on dementia and other diseases of aging. The investments in longitudinal cohort studies like ARIC will benefit all of us for many years to come.”

In the future, Dr. Gottesman and her team plan to investigate ways in which subclinical, or undiagnosed, vascular problems may influence the brain and why race is associated with dementia.



Story Source:

Materials provided by NIH/National Institute of Neurological Disorders and StrokeNote: Content may be edited for style and length.

Journal Reference:

Gottesman et al. Associations Between Midlife Vascular Risk Factors and 25-Year Incident Dementia in the Atherosclerosis Risk in Communities (ARIC) CohortJAMA Neurology, August 7, 2017 DOI: 10.1001/jamaneurol.2017.1658

Copyright 2017 ScienceDaily or by third parties, where indicated.


How Physical Exercise Prevents Dementia

(Goethe-Universität Frankfurt am Main) Numerous studies have shown that physical exercise seems beneficial in the prevention of cognitive impairment and dementia in old age. Now researchers at Goethe University Frankfurt have explored in one of the first studies worldwide how exercise affects brain metabolism.

In order to further advance current state of knowledge on the positive influence of physical activity on the brain, gerontologists and sports physicians at Goethe University Frankfurt have examined the effects of regular exercise on brain metabolism and memory of 60 participants aged between 65 and 85 in a randomised controlled trial. Their conclusion: regular physical exercise not only enhances fitness but also has a positive impact on brain metabolism.

As the researchers report in the current issue of the medical journal Translational Psychiatry, they thoroughly examined all the participants in the SMART study (Sport and Metabolism in Older Persons, an MRT Study) by assessing movement-related parameters, cardiopulmonary fitness and cognitive performance. In addition, magnetic resonance tomography (MRT) and magnetic resonance spectroscopy (MRS) were used to measure brain metabolism and brain structure.

Following this examination, the participants mounted an exercise bike three times a week over a period of 12 weeks. The 30-minute training sessions were individually adapted to each participant’s performance level. The participants were examined again after the end of the programme in order to document the effects of this physical activity on brain metabolism, cognitive performance and brain structure.

The researchers also investigated to what extent exercise had led to an improvement in the participants’ physical fitness. The study was conducted by the Gerontology Department of the Institute of General Medicine (headed by Professor Johannes Pantel) and the Department of Sports Medicine (led by Professor Winfried Banzer).

As expected, physical activity had influenced brain metabolism: it prevented an increase in choline. The concentration of this metabolite often rises as a result of the increased loss of nerve cells, which typically occurs in the case of Alzheimer’s disease. Physical exercise led to stable cerebral choline concentrations in the training group, whereas choline levels increased in the control group. The participants’ physical fitness also improved: they showed increased cardiac efficiency after the training period.

Overall, these findings suggest that physical exercise not only improves physical fitness but also protects cells.



Journal Reference:

S Matura, J Fleckenstein, R Deichmann, T Engeroff, E Füzéki, E Hattingen, R Hellweg, B Lienerth, U Pilatus, S Schwarz, V A Tesky, L Vogt, W Banzer, J Pantel. Effects of aerobic exercise on brain metabolism and grey matter volume in older adults: results of the randomised controlled SMART trial. Translational Psychiatry, 2017; 7 (7): e1172 DOI: 10.1038/tp.2017.135

Copyright 2017 ScienceDaily or by third parties, where indicated.



Alzheimer’s Association International Conference 2017: Wrap Up

(Alzheimer’s Association) The Alzheimer’s Association today announced the launch of a $20 million U.S. two- year clinical trial to test the ability of a multi-dimensional lifestyle intervention to prevent cognitive decline and dementia in 2,500 older adults with no current cognitive symptoms but who are at increased risk for later cognitive decline. The announcement was made at the 2017 Alzheimer’s Association International Conference (AAIC 2017) in London.

The large U.S. study to PrOtect through a lifestyle INTErvention to Reduce risk (US POINTER) will include physical exercise, nutritional counseling and modification, cognitive and social stimulation, and improved self- management of medical conditions. Recruiting for the study will begin in 2018.

At AAIC 2014, Miia Kivipelto, M.D., Ph.D., Professor at the Karolinska Institutet, Sweden and the National Institute for Health and Welfare, Helsinki, Finland, and colleagues reported on the results of the FINGER Study – the first randomized controlled trial showing that it is possible to prevent cognitive decline using a multi-domain lifestyle intervention among older at-risk individuals. The results highlighted the value of addressing multiple dementia risk factors as a strategy to protect brain health. The FINGER model is now being replicated in the United States, Europe, Singapore, and Australia – including people from a variety of geographical and cultural backgrounds.

“We now can effectively prevent and treat heart disease with a combination of drugs and lifestyle. The same is true with some cancers; the same with HIV/AIDS. The same may also be true for Alzheimer’s disease and other dementias in the not too distant future,” said Maria C. Carrillo, PhD, Alzheimer’s Association Chief Science Officer.

“We must test all options to treat and prevent this horrible disease. We must find the answers for the millions dying with Alzheimer’s and their families, and the tens of millions more who will become affected if we do not act now. The Alzheimer’s Association is extremely proud to launch this clinical trial with our scientific partners,” Carrillo said.

Also announced today at AAIC 2017:

  • Interim results of the IDEAS Study, which is testing the impact on medical management of brain PET scans to detect amyloid protein. Amyloid forms the hallmark brain plaques of Alzheimer’s disease.
  • A possible blood marker for amyloid build up in the brain.
  • New insights into how amyloid and tau proteins spread through the brains of people with Alzheimer’s. Abnormal tau forms brain tangles – the other hallmark lesion of Alzheimer’s.

U.S. study to PrOtect through a lifestyle INTErvention to Reduce risk (US POINTER)

Increasing age is the greatest risk factor for Alzheimer’s disease. With the aging of the global population – and the slow progress of developing and testing drug treatments – prevention is pivotal in managing the inexorable rise in global cases of Alzheimer’s and other dementias.

In 2014, a large-scale two-year study in Finland in healthy older adults at increased risk of cognitive decline and dementia (the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability, or FINGER Study) found that a two-year combination therapy involving physical exercise, nutrition, cognitive stimulation, and self-monitoring of heart health risk factors had a protective effect on cognitive function. These results were first reported at AAIC 2014 in Copenhagen.

According to Co-Principal Investigator Laura Baker, PhD, of the Wake Forest School of Medicine, Winston- Salem, North Carolina, the U.S. study to PrOtect through a lifestyle INTErvention to Reduce risk (US POINTER) is modeled on the FINGER study. It will test whether two years of a combined intervention that includes physical exercise, nutritional counseling and modification, cognitive and social stimulation, and improved self- management of medical co-morbidities benefits cognitive function in older adults at increased risk of cognitive decline and dementia. The comparison group will receive health education and support through in-person group meetings on health- and aging-related topics, and annual feedback on laboratory tests.

Starting in 2018, 2,500 study participants 60-79 years old will be identified using a medical record search to select those with medical conditions that have been linked to an increased risk for dementia (e.g., hypertension and other cardiovascular events, elevated blood sugar). Information about family history of Alzheimer’s, physical activity level, and current cognitive status and mood will be collected in follow-up interviews to further identify eligible participants. Local Alzheimer’s Association offices nationwide will participate in intervention delivery. National partnerships will be developed with community-based organizations to deliver the exercise, nutrition, social and medical aspects of the intervention.

The success of the intervention will be evaluated based on two-year change in a global measure of cognitive function focused on short-term memory, attention and concentration.

“As of now, there are no approved medications that have produced results similar to the FINGER Study. There is a pressing need to test the effectiveness of a multicomponent lifestyle intervention in larger and more diverse populations, such as the United States,” said Baker. “The lifestyle intervention in US POINTER is an important multi-dimensional strategy to protect brain health and potentially reduce risk of dementia.”

An update on FINGER and overviews of the Singapore (SINGER) and Australia (Maintain Your Brain) prevention studies will also be reported at AAIC 2017. The worldwide effort, collectively referred to as WW- FINGERS, supports a collaborative network of trials and experienced investigators to facilitate harmonization of research methods, and sharing of experiences and data for maximum global scientific impact.

Clinical Impact of Brain Amyloid PET Scans – Interim Results from the IDEAS Study

Launched in 2016, the four-year Imaging Dementia-Evidence for Amyloid Scanning (IDEAS) study is evaluating the impact of brain amyloid PET scans on patient management and health outcomes. Participants are more than 18,000 Medicare beneficiaries age 65+ with mild cognitive impairment (MCI) or atypical dementia who meet published Appropriate Use Criteria (AUC) for clinical amyloid PET. Before brain amyloid PET scans – which detect amyloid plaques, a core feature of Alzheimer’s – amyloid plaques could be seen only during autopsies, making it much harder to give living patients a definitive diagnosis.

At AAIC 2017, Principal Investigator Gil Rabinovici, MD, of the Memory and Aging Center, University of California, San Francisco, and colleagues reported early results from IDEAS assessing changes in patient management in the first 3,979 participants for whom case report forms were completed by participating dementia specialists both before and 90 days after the PET scans.

The pre-PET form documented the specialist’s management plan assuming no access to amyloid PET; the post- PET form recorded the medical management plan approximately 90 days after receiving results from a brain amyloid PET with an FDA-approved beta-amyloid imaging agent.

The researchers measured the rate of change between pre- and post-PET medical management, including one or more of: Alzheimer’s disease drug therapy, other drug therapy, and counseling about safety and future planning. Participants’ median age was 75 (range: 65-95); 64.4% were diagnosed with MCI, 35.6% met criteria for dementia. The most common suspected cause of cognitive impairment prior to PET was Alzheimer’s disease (76.3%). Rates of amyloid PET positivity were 54.3% in MCI and 70.5% in dementia.

Changes in medical management were seen in 67.8% of MCI patients (47.8% change in AD drugs, 36.0% change in other drugs, 23.9% changes in counseling), and in 65.9% of dementia patients (47.7% change in AD drugs, 32.2% change in other drugs, 15.3% change in counseling). Amyloid PET scans also reduced the need for additional diagnostic testing such as neuropsychological testing (from 26.3% recommended pre-PET to 11.0% recommended post-PET) and spinal fluid testing (from 10.5% to 1.0%).

“Our original hypothesis was that having amyloid PET scan results would change medical management in 30 percent of cases,” Rabinovici said. “Our interim results suggest we are well on track to see an effect of at least that magnitude, and perhaps greater, when the final results are available.”

“We look forward to reporting the results from the full study population. We are very grateful to the Centers for Medicare & Medicaid Services for their support of the IDEAS Study as our results indicate that access to this technology is making a real difference in the care of patients,” Rabinovici added.

The IDEAS Study is led by the Alzheimer’s Association and managed by the American College of Radiology.

The IDEAS Study was developed in response to CMS’ 2013 National Coverage Decision (NCD) on amyloid PET imaging in dementia and neurodegenerative disease (CAG-00431N) not to cover the scans because “the evidence is insufficient to conclude that the use of positron emission tomography (PET) amyloid-beta (Aβ) imaging is reasonable and necessary for the diagnosis or treatment of illness or injury or to improve the functioning of … Medicare beneficiaries with dementia or neurodegenerative disease.” Under the NCD, Medicare will provide coverage for one amyloid PET scan per patient enrolled in an approved clinical study.

A working group convened by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging (SNMMI) developed AUC for brain amyloid PET scans. The AUC indicate that amyloid PET should only be considered in patients with clear, measurable cognitive deficits when there is substantial diagnostic uncertainty after a comprehensive evaluation by a dementia specialist. According to AUC, amyloid PET may have greatest value in patients with either: (1) progressive, unexplained mild cognitive impairment (MCI); or (2) dementia of uncertain cause due to atypical or mixed symptoms, or unusually early age-of-onset.

A Blood Biomarker for Amyloid Plaques?

There is substantial evidence implicating amyloid-beta in the cause and/or progression of Alzheimer’s disease. Currently, a spinal tap or PET scan can detect deposition of amyloid in the brain, which precedes and increases the risk of progression to Alzheimer’s disease dementia. However, due to the invasiveness of a spinal tap and the radioactivity, limited availability and cost of PET scans, there is an urgent need for a simpler, more practical test for amyloid deposition, such as a blood test.

In order to investigate a blood-based amyloid biomarker, Randall Bateman, MD, and scientists at Washington University School of Medicine in St. Louis adapted their previously reported Stable Isotope Label Kinetics (SILK) method to measure amyloid in the blood – how fast it is created and how fast it is cleared away.

Participants were 41 older adults either with or without amyloidosis in the brain; they had either clinically diagnosed late-onset Alzheimer’s or were cognitively normal age-matched controls. All participants had brain PET amyloid imaging and/or cerebrospinal fluid (CSF) amyloid measures to detect brain amyloidosis. Blood sampling was conducted over 24 hours, and analyzed in a blinded fashion so researchers didn’t know which samples were from amyloid positive or amyloid negative people.

The scientists found the longer, stickier form of amyloid (known as Aβ42) was created and removed significantly faster in amyloid positive participants compared to amyloid negative participants. The findings were similar to prior studies done in CSF, suggesting that the amyloid levels detected in blood can accurately reflect the amyloid buildup in the brain. Additional results of a larger validation study will also be reported at AAIC 2017.

“These findings are important because they support the idea that blood amyloid interacts with and is derived from the brain,” Bateman said.

“We’re excited because the results also suggest that blood-derived amyloid-beta may be useful as a rapid and inexpensive screening test for brain amyloidosis, and may be able to identify people who are at higher risk of Alzheimer’s disease very early in the process.”

“Having a simple and inexpensive blood test for screening is likely to greatly accelerate clinical trials to find Alzheimer’s drugs. And, it could facilitate widespread treatment when effective anti-amyloid therapeutics are developed,” Bateman added.

“We envision that one day soon, as part of a regular screening for cholesterol and blood pressure, a person may also get a blood test to find out if the amyloid protein is building up in the brain, and then go on specific treatments to prevent the onset of Alzheimer’s disease dementia. This would be similar to the already successful approach of screening for and treating high cholesterol to reduce the risk of heart attacks and strokes.”

This research was supported by an Alzheimer’s Association Zenith award grant and an NIH R01 study.

Amyloid and Tau Spreading Pathways in the Brain, Correlated with Genetics

The ability to employ advanced imaging technology to “see” both of the hallmark proteins of Alzheimer’s (amyloid and tau) in the living brain is a significant recent advance in the field. It may prove to be transformational not only in our understanding of the disease and its progression but also in its potential to accelerate drug discovery.

According to Jorge Sepulcre, MD, PhD, of Massachusetts General Hospital and Harvard Medical School, Boston, understanding the “spreading” phenomenon of abnormal tau and amyloid-beta proteins in the brain is critical to knowing what is causing the devastating cell damage and relentless symptoms of people with Alzheimer’s.

Sepulcre and colleagues developed a novel imaging approach to investigate the spreading pathways of tau and amyloid deposits over time, as well as their genetic vulnerabilities, in a longitudinal sample of elderly participants in the Harvard Aging Brain Study. Eighty-eight (88) study participants, average age about 76, were divided into two independent samples: (1) a cross-sectional sample of 69 people; and (2) a 1-2 year follow-up longitudinal sample of 19 subjects.

The researchers found that tau and amyloid appear to accumulate along distinctive pathways in the brain; the same communication pathways, or neural networks, we use for daily brain function. According to their findings, tau – which we know starts in the middle of the brain memory center – spreads forward and out toward the front of the brain. Amyloid, which starts in the back of the brain, spreads further back and outward from the middle. Specifically:

  • Medial/inferior temporal lobe areas project pathways of Tau-spreading toward anterior pole, lateral and posteriomedial temporal cortex, and orbitofrontal cortex.
  • Posterior cingulate cortex spreads Aβ toward surrounding areas and lateral parietal lobe.

The scientists discovered that 354 genes were significantly associated with the tau spreading pathway, including the MAPT gene, which was previously associated with Alzheimer’s disease risk. They also found 216 genes, including the CLU gene, significantly associated with the amyloid pathway. Additional analysis characterized the tau spreading genetic profile as “axon-related” and the amyloid-spreading genetic profile as “dendrite-related”. APOE, the gene with the highest impact on Alzheimer’s risk, was found to be the most central gene linking tau- and amyloid-spreading pathways.

“Our results reported at AAIC 2017 suggest that tau and amyloid advance through different brain systems over time,” Sepulcre said. “We also discovered certain genetic traits that may confer tau or amyloid vulnerability in the brain.”

“The findings may improve our ability to track responses to potential therapeutic interventions in the future,” Sepulcre added. “In addition, when more effective drug therapies become available, these results may help doctors determine which patients should get which therapies, and the optimum time to take them.”

About Alzheimer’s Association International Conference (AAIC)
The Alzheimer’s Association International Conference (AAIC) is the world’s largest gathering of researchers from around the world focused on Alzheimer’s and other dementias. As a part of the Alzheimer’s Association’s research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community.
AAIC 2017 home page: www.alz.org/aaic/
AAIC 2017 newsroom: www.alz.org/aaic/press.asp

About the Alzheimer’s Association®
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer’s care, support and research. Our mission is to eliminate Alzheimer’s disease through the advancement of research, to provide and enhance care and support for all affected and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. Visit alz.org or call +1 800.272.3900.



  • Laura D. Baker, PhD, et al. U.S. Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (US- FINGER). (Funder: Alzheimer’s Association)
  • Gil D Rabinovici, MD, et al. Impact of Amyloid PET on Patient Management: Early Results from the IDEAS Study. (Funder(s): U.S. Center for Medicare and Medicaid Services, Alzheimer’s Association, Eli Lilly, GE Healthcare, Piramal)
  • Randall J Bateman, MD, et al. Concentrations and Stable Isotope Label Kinetics of Human Plasma Amyloid Beta. (Funder(s): U.S. National Institutes of Health, Alzheimer’s Association)
  • Jorge Sepulcre, MD, PhD, et al. In Vivo spreading Pathways of Tau and Amyloid Accumulation and Its Genetic Underpinnings. (Funder(s): U.S. National Institutes of Health, Alzheimer’s Association)



Sleep Problems May Be Early Sign of Alzheimer’s

(American Academy of Neurology) Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer’s disease later in life than people who do not have sleep problems, according to a study published in the July 5, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. Researchers have found a link between sleep disturbances and biological markers for Alzheimer’s disease found in the spinal fluid.

“Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison.

“For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”

Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.

For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer’s disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.

Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer’s disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.

“It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending,” said Bendlin.

While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.

The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.

“It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep,” said Bendlin. “More research is needed to further define the relationship between sleep and these biomarkers.”

Bendlin added, “There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”

One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.

The American Academy of Neurology is the world’s largest association of neurologists and neuroscience professionals, with 32,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.



©2017 American Academy of Neurology – All Rights Reserved


Brains Evolved to Need Exercise

(University of Arizona) Mounting scientific evidence shows that exercise is good not only for our bodies, but for our brains. Yet, exactly why physical activity benefits the brain is not well understood.

In a new article published in the journal Trends in Neurosciences, University of Arizona researchers suggest that the link between exercise and the brain is a product of our evolutionary history and our past as hunter-gatherers.

UA anthropologist David Raichlen and UA psychologist Gene Alexander, who together run a research program on exercise and the brain, propose an “adaptive capacity model” for understanding, from an evolutionary neuroscience perspective, how physical activity impacts brain structure and function.

Their argument: As humans transitioned from a relatively sedentary apelike existence to a more physically demanding hunter-gatherer lifestyle, starting around 2 million years ago, we began to engage in complex foraging tasks that were simultaneously physically and mentally demanding, and that may explain how physical activity and the brain came to be so connected.

“We think our physiology evolved to respond to those increases in physical activity levels, and those physiological adaptations go from your bones and your muscles, apparently all the way to your brain,” said Raichlen, an associate professor in the UA School of Anthropology in the College of Social and Behavioral Sciences.

“It’s very odd to think that moving your body should affect your brain in this way — that exercise should have some beneficial impact on brain structure and function — but if you start thinking about it from an evolutionary perspective, you can start to piece together why that system would adaptively respond to exercise challenges and stresses,” he said.

Having this underlying understanding of the exercise-brain connection could help researchers come up with ways to enhance the benefits of exercise even further, and to develop effective interventions for age-related cognitive decline or even neurodegenerative diseases such as Alzheimer’s.

Notably, the parts of the brain most taxed during a complex activity such as foraging — areas that play a key role in memory and executive functions such as problem solving and planning — are the same areas that seem to benefit from exercise in studies.

“Foraging is an incredibly complex cognitive behavior,” Raichlen said.

“You’re moving on a landscape, you’re using memory not only to know where to go but also to navigate your way back, you’re paying attention to your surroundings. You’re multitasking the entire time because you’re making decisions while you’re paying attention to the environment, while you are also monitoring your motor systems over complex terrain. Putting all that together creates a very complex multitasking effort.”

The adaptive capacity model could help explain research findings such as those published by Raichlen and Alexander last year showing that runners’ brains appear to be more connected than brains of non-runners.

The model also could help inform interventions for the cognitive decline that often accompanies aging — in a period in life when physical activity levels tend to decline as well.

“What we’re proposing is, if you’re not sufficiently engaged in this kind of cognitively challenging aerobic activity, then this may be responsible for what we often see as healthy brain aging, where people start to show some diminished cognitive abilities,” said Alexander, a UA professor of psychology, psychiatry, neuroscience and physiological sciences.

“So the natural aging process might really be part of a reduced capacity in response to not being engaged enough.”

Reduced capacity refers to what can happen in organ systems throughout the body when they are deprived of exercise.

“Our organ systems adapt to the stresses they undergo,” said Raichlen, an avid runner and expert on running.

“For example, if you engage in exercise, your cardiovascular system has to adapt to expand capacity, be it through enlarging your heart or increasing your vasculature, and that takes energy. So if you’re not challenging it in that way — if you’re not engaging in aerobic exercise — to save energy, your body simply reduces that capacity.”

In the case of the brain, if it is not being stressed enough it may begin to atrophy. This may be especially concerning, considering how much more sedentary humans’ lifestyles have become.

“Our evolutionary history suggests that we are, fundamentally, cognitively engaged endurance athletes, and that if we don’t remain active we’re going to have this loss of capacity in response to that,” said Alexander, who studies brain aging and Alzheimer’s disease as a member of the UA’s Evelyn F. McKnight Brain Institute.

“So there really may be a mismatch between our relatively sedentary lifestyles of today and how we evolved.”

Alexander and Raichlen say future research should look at how different levels of exercise intensity, as well as different types of exercise, or exercise paired specifically with cognitive tasks, affect the brain.

For example, exercising in a novel environment that poses a new mental challenge, may prove to be especially beneficial, Raichlen said.

“Most of the research in this area puts people in a cognitively impoverished environment. They put people in a lab and have them run on a treadmill or exercise bike, and you don’t really have to do as much, so it’s possible that we’re missing something by not increasing novelty,” he said.

Alexander and Raichlen say they hope the adaptive capacity model will help advance research on exercise and the brain.

“This evolutionary neuroscience perspective is something that’s been generally lacking in the field,” Alexander said.

“And we think this might be helpful to advance research and help develop some new specific hypotheses and ways to identify more universally effective interventions that could be helpful to everyone.”



Journal Reference:

David A. Raichlen, Gene E. Alexander. Adaptive Capacity: An Evolutionary Neuroscience Model Linking Exercise, Cognition, and Brain Health. Trends in Neurosciences, 2017; 40 (7): 408 DOI: 10.1016/j.tins.2017.05.001

Copyright 2017 ScienceDaily or by third parties, where indicated. All rights controlled by their respective owners.



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.



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© 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.

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© 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.”



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