A study of nearly 2,500 adults found that having trouble falling asleep, as compared to other patterns of insomnia, was the main insomnia symptom that predicted cognitive impairment 14 years later.
Results show that having trouble falling asleep in 2002 was associated with cognitive impairment in 2016. Specifically, more frequent trouble falling asleep predicted poorer episodic memory, executive function, language, processing speed, and visuospatial performance. Further analysis found that associations between sleep initiation and later cognition were partially explained by both depressive symptoms and vascular diseases in 2014 for all domains except episodic memory, which was only partially explained by depressive symptoms.
“While there is growing evidence for a link between insomnia and cognitive impairment in older adults, it has been difficult to interpret the nature of these associations given how differently both insomnia and cognitive impairment can present across individuals,” said lead author Afsara Zaheed, a graduate student in clinical science within the department of psychology at the University of Michigan. “By investigating associations between specific insomnia complaints and cognition over time using strong measures of cognitive ability, we hoped to gain additional clarity on whether and how these different sleep problems may lead to poor cognitive outcomes.”
Insomnia involves difficulty falling asleep or staying asleep, or regularly waking up earlier than desired, despite allowing enough time in bed for sleep. Daytime symptoms include fatigue or sleepiness; feeling dissatisfied with sleep; having trouble concentrating; feeling depressed, anxious, or irritable; and having low motivation or energy.
Researchers have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them.
Researchers at Albert Einstein College of Medicine have designed an experimental drug that reversed key symptoms of Alzheimer’s disease in mice. The drug works by reinvigorating a cellular cleaning mechanism that gets rid of unwanted proteins by digesting and recycling them. The study was published online today in the journal Cell.
“Discoveries in mice don’t always translate to humans, especially in Alzheimer’s disease,” said co-study leader Ana Maria Cuervo, M.D., Ph.D., the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases, professor of developmental and molecular biology, and co-director of the Institute for Aging Research at Einstein. “But we were encouraged to find in our study that the drop-off in cellular cleaning that contributes to Alzheimer’s in mice also occurs in people with the disease, suggesting that our drug may also work in humans.” In the 1990s, Dr. Cuervo discovered the existence of this cell-cleaning process, known as chaperone-mediated autophagy (CMA) and has published 200 papers on its role in health and disease.
CMA becomes less efficient as people age, increasing the risk that unwanted proteins will accumulate into insoluble clumps that damage cells. In fact, Alzheimer’s and all other neurodegenerative diseases are characterized by the presence of toxic protein aggregates in patients’ brains. The Cell paper reveals a dynamic interplay between CMA and Alzheimer’s disease, with loss of CMA in neurons contributing to Alzheimer’s and vice versa. The findings suggest that drugs for revving up CMA may offer hope for treating neurodegenerative diseases.
Scientists have more evidence that exercise improves brain health and could be a lifesaving ingredient that prevents Alzheimer’s disease.
In particular, a new study from the University of Texas (UT) Southwestern’s O’Donnell Brain Institute suggests that the lower the fitness level, the faster the deterioration of vital nerve fibers in the brain. This deterioration results in cognitive decline, including memory issues characteristic of dementia patients.
“This research supports the hypothesis that improving people’s fitness may improve their brain health and slow down the aging process,” said Dr. Kan Ding, a neurologist from the Peter O’Donnell Jr. Brain Institute who authored the study.
The study published in the Journal of Alzheimer’s Disease focused on a type of brain tissue called white matter, which is comprised of millions of bundles of nerve fibers used by neurons to communicate across the brain.
Dr. Ding’s team enrolled older patients at high risk to develop Alzheimer’s disease who have early signs of memory loss, or mild cognitive impairment (MCI). The researchers determined that lower fitness levels were associated with weaker white matter, which in turn correlated with lower brain function.
Unlike previous studies that relied on study participants to assess their own fitness, the new research objectively measured cardiorespiratory fitness with a scientific formula called maximal oxygen uptake. Scientists also used brain imaging to measure the functionality of each patient’s white matter.
Patients were then given memory and other cognitive tests to measure brain function, allowing scientists to establish strong correlations between exercise, brain health, and cognition.
The study adds to a growing body of evidence pointing to a simple yet crucial mandate for human health: Exercise regularly.
However, the study leaves plenty of unanswered questions about how fitness and Alzheimer’s disease are intertwined. For instance, what fitness level is needed to notably reduce the risk of dementia? Is it too late to intervene when patients begin showing symptoms?
Some of these topics are already being researched through a five-year national clinical trial led by the O’Donnell Brain Institute.
The trial, which includes six medical centers across the country, aims to determine whether regular aerobic exercise and taking specific medications to reduce high blood pressure and cholesterol levels can help preserve brain function. It involves more than 600 older adults at high risk to develop Alzheimer’s disease.
“Evidence suggests that what is bad for your heart is bad for your brain. We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer’s disease,” said Dr. Rong Zhang of UT Southwestern, who oversees the clinical trial and is Director of the Cerebrovascular Laboratory in the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas, where the Dallas arm of the study is being carried out.
The research builds upon prior investigations linking healthy lifestyles to better brain function, including a 2013 study from Dr. Zhang’s team that found neuronal messages are more efficiently relayed in the brains of older adults who exercise.
In addition, other teams at the O’Donnell Brain Institute are designing tests for the early detection of patients who will develop dementia, and seeking methods to slow or stop the spread of toxic proteins associated with the disease such as beta-amyloid and tau, which are blamed for destroying certain groups of neurons in the brain.
“A lot of work remains to better understand and treat dementia,” said Dr. Ding, Assistant Professor of Neurology & Neurotherapeutics. “But, eventually, the hope is that our studies will convince people to exercise more.
For years, research to pin down the underlying cause of Alzheimer’s Disease has been focused on plaque found to be building up in the brain in AD patients. But treatments targeted at breaking down that buildup have been ineffective in restoring cognitive function, suggesting that the buildup may be a side effect of AD and not the cause itself.
A new study led by a team of Brigham Young University (BYU) researchers finds novel cellular-level support for an alternate theory that is growing in strength: Alzheimer’s could actually be a result of metabolic dysfunction in the brain. In other words, there is growing evidence that diet and lifestyle are at the heart of Alzheimer’s Disease.
“Alzheimer’s Disease is increasingly being referred to as insulin resistance of the brain or Type 3 Diabetes,” said senior study author Benjamin Bikman, a professor of physiology and developmental biology at BYU. “Our research shows there is likely a lifestyle origin to the disease, at least to some degree.”
Because of the dementia and Alzheimer’s Disease that have affected my family on both sides, I remain acutely aware of developments in addressing cognition in the aging population. So, this study reported in Science Daily resonated with me.
A two-week course of high doses of CBD helps restore the function of two proteins key to reducing the accumulation of beta-amyloid plaque, a hallmark of Alzheimer’s disease, and improves cognition in an experimental model of early onset familial Alzheimer’s, investigators report.
The proteins TREM2 and IL-33 are important to the ability of the brain’s immune cells to literally consume dead cells and other debris like the beta-amyloid plaque that piles up in patients’ brains, and levels of both are decreased in Alzheimer’s.
The investigators report for the first time that CBD normalizes levels and function, improving cognition as it also reduces levels of the immune protein IL-6, which is associated with the high inflammation levels found in Alzheimer’s, says Dr. Babak Baban, immunologist and associate dean for research in the Dental College of Georgia and the study’s corresponding author.
There is a dire need for novel therapies to improve outcomes for patients with this condition, which is considered one of the fastest-growing health threats in the United States, DCG and Medical College of Georgia investigators write in the Journal of Alzheimer’s Disease.
Exercise may reduce decline in global cognition in older adults with mild-to-moderate AD dementia. Aerobic exercise did not show superior cognitive effects to stretching in our pilot trial, possibly due to the lack of power. ASU Edson College of Nursing and Health Innovation Professor Fang Yu led a pilot randomized control trial that included 96 older adults living with mild to moderate Alzheimer’s dementia.
Participants were randomized to either a cycling (stationary bike) or stretching intervention for six months. Using the Alzheimer’s Disease Assessment Scale-Cognition (ADAS-Cog) to assess cognition, the results of the trial were substantial.
The six-month change in ADAS-Cog was 1.0±4.6 (cycling) and 0.1±4.1 (stretching), which were both significantly less than the expected 3.2±6.3-point increase observed naturally with disease progression.
“Our primary finding indicates that a six-month aerobic exercise intervention significantly reduced cognitive decline in comparison to the natural course of changes for Alzheimer’s dementia. However, we didn’t find a superior effect of aerobic exercise to stretching, which is likely due to the pilot nature of our trial. We don’t have the statistical power to detect between-group differences, there was substantial social interaction effect in the stretching group, and many stretching participants did aerobic exercise on their own.” Yu said.
The findings are described in a recently published article, Cognitive Effects of Aerobic Exercise in Alzheimer’s Disease: A Pilot Randomized Controlled Trial, in the Journal of Alzheimer’s Disease.
Yu says their results are encouraging and support the clinical relevance of promoting aerobic exercise in individuals with Alzheimer’s dementia to maintain cognition.
“Aerobic exercise has a low profile of adverse events in older adults with Alzheimer’s dementia as demonstrated by our trial,” said Yu. “Regardless of its effect on cognition, the current collective evidence on its benefits supports the use of aerobic exercise as an additional therapy for Alzheimer’s disease.”
Working in the paid labor workforce may have cognitive benefits later in life for U.S. women. For a study supported in part by the National Institute on Aging (NIA), researchers looked at the influence of social, employment, and gender-related factors on memory decline with implications for dementia risk. Their findings, recently published in Neurology, show that women in the workforce during early adulthood and midlife experienced slower rates of memory decline than those who had not worked for pay.
A team of University of California (UC), Los Angeles; UC San Francisco; Harvard; and Boston College researchers analyzed the employment patterns, family structure, and demographic characteristics of U.S. women. More than 6,000 women at least age 55 in the Health and Retirement Study reported their past work-family statuses of employment, marriage, and parenthood between ages 16 and 50. They also participated in word recall memory assessments every two years over an average of 12 years. The study team then evaluated rates of later-life memory decline, which is a measure associated with dementia.
The average rate of memory decline after age 60 was slower for women who had worked, regardless of marriage and parenthood status. Taking time off from work when their children were young did not seem to decrease the cognitive benefit in married working mothers. Among nonworking mothers, rates of memory decline were similar for single and married women. Demographic characteristics, such as race, childhood socioeconomic status, and level of education, did not explain the relationship between work-family status and memory decline.
This study adds to evidence that participation in the workforce may be a protective factor for cognitive health later in life. The researchers did not look at volunteer work, the types of paid labor among women, or possible differences among genders. Future research on effects of participating in the workforce, such as cognitive stimulation and social engagement, may help explain how employment can decrease the rate of memory loss.
Eat less; move more; live longer and keep cognition – words to live by.
New research from the University of Sheffield has found being overweight is an additional burden on brain health and it may exacerbate Alzheimer’s Disease.
The pioneering multi-modal neuro-imaging study revealed obesity may contribute toward neural tissue vulnerability, whilst maintaining a healthy weight in mild Alzheimer’s disease dementia could help to preserve brain structure.
The findings, published in The Journal of Alzheimer’s Disease Reports, also highlight the impact being overweight in mid-life could have on brain health in older age.
Lead author of the study, Professor Annalena Venneri from the University of Sheffield’s Neuroscience Institute and NIHR Sheffield Biomedical Research Centre, said: “More than 50 million people are thought to be living with Alzheimer’s disease and despite decades of ground breaking studies and a huge global research effort we still don’t have a cure for this cruel disease.
Today, cognitive impairment and ADRD are major global public health and social concerns as the population of older adults rises around the world. By 2050, more than 152 million people will be affected by these conditions. That’s why many countries, including the United States, see the prevention of ADRD as a key public health priority and are studying programs to help stem these diseases.
One way to prevent cognitive impairment and ADRD is to treat the problems that raise the risk for developing them. Two of these risk factors are hearing and vision loss. Currently, about 60 percent of people aged 70 years or older are affected by hearing loss, 40 percent are affected by vision loss, and 23 percent of older adults have both vision and hearing loss. Some studies have suggested that having both hearing and vision loss may be linked to poorer cognitive function or to a faster rate of cognitive decline.
Apathy – a lack of interest or motivation – could predict the onset of some forms of dementia many years before symptoms start, offering a ‘window of opportunity’ to treat the disease at an early stage, according to new research from a team of scientists led by Professor James Rowe at the University of Cambridge.
Frontotemporal dementia is a significant cause of dementia among younger people. It is often diagnosed between the ages of 45 and 65. It changes behavior, language and personality, leading to impulsivity, socially inappropriate behavior, and repetitive or compulsive behaviors.
A common feature of frontotemporal dementia is apathy, with a loss of motivation, initiative and interest in things. It is not depression, or laziness, but it can be mistaken for them. Brain-scanning studies have shown that in people with frontotemporal dementia it is caused by shrinkage in special parts at the front of the brain – and the more severe the shrinkage, the worse the apathy. But, apathy can begin decades before other symptoms, and be a sign of problems to come.
The foods we eat may have a direct impact on our cognitive acuity in our later years. This is the key finding of an Iowa State University research study spotlighted in an article published in the November 2020 issue of the Journal of Alzheimer’s Disease.
The study was spearheaded by principal investigator, Auriel Willette, an assistant professor in Food Science and Human Nutrition, and Brandon Klinedinst, a Neuroscience PhD candidate working in the Food Science and Human Nutrition department at Iowa State. The study is a first-of-its-kind large scale analysis that connects specific foods to later-in-life cognitive acuity.
Alzheimer’s disease and other forms of dementia affect millions of older adults in the US—but not equally. Past research has identified risk factors including genes, education, racism, and air pollution, and a growing number of studies now point to noise as another influence on risk of dementia.
Now, a new study co-led by a School of Public Health researcher finds that 10 decibels more daytime neighborhood noise is associated with 36 percent higher odds of mild cognitive impairment and 30 percent higher odds of Alzheimer’s disease.
“We remain in early stages in researching noise and dementia, but the signals so far, including those from our study, suggest we should pay more attention to the possibility that noise affects cognitive risk as we age,” says study first author Jennifer Weuve, associate professor of epidemiology.
A new study from Lund University in Sweden shows that validated biomarkers can reveal an individual’s risk of developing Alzheimer’s disease. Using a model that combines the levels of two specific proteins in the blood of those with mild memory impairment, the researchers are able to predict the risk of developing Alzheimer’s. The researchers have also developed an app that doctors can use to give patients a risk assessment.
Oskar Hansson and his colleagues have been researching different biomarkers for a long time to produce better diagnostics at an early stage of Alzheimer’s disease. Over the past year, they have also developed accurate markers in blood tests for Alzheimer’s. The aim has been to identify the disease at an early stage of its progression, before the actual dementia stage, in order to begin treatment to ease symptoms, avoid unnecessary examinations and create a sense of security among patients.
Falls are the leading cause of fatal injuries in older adults, causing more than 800,000 hospitalizations and about 30,000 deaths in the U.S. every year. Some risk factors are well-known — advanced age, problems with vision or balance, muscle weakness — but an under-recognized factor is early Alzheimer’s disease. Older people in the earliest stages of Alzheimer’s, before cognitive problems arise, are more likely to suffer a fall than people who are not on track to develop dementia.
Researchers at Washington University School of Medicine in St. Louis have found that, in older people without cognitive problems who experience a fall, the process of neuro-degeneration that leads to Alzheimer’s dementia already may have begun. The findings, available online in the Journal of Alzheimer’s Disease, suggest that older people who have experienced falls should be screened for Alzheimer’s and that new strategies may be needed to reduce the risk of falling for people in the disease’s early stages.
Subtle differences in cognition may help identify individuals at risk for becoming dependent years later upon others to complete daily activities, such as managing medications or finances and other essential activities.
Writing in the September 29, 2020 online issue of the Journal of Alzheimer’s Disease, researchers at University of California San Diego School of Medicine, with colleagues elsewhere, linked poorer cognitive performance in a single testing with subsequent greater risk for impaired daily life activities nearly a decade later.
The study involved a diverse but understudied cohort of Latinos living in the United States. Outcomes were most severe for individuals 70 years and older, but gender and ethnic background, such as Mexican or Puerto Rican, were not significant differentiators. The authors said the findings in sum highlight the need for early preventive care across Latinos and Latinas of various backgrounds.
A new analysis published in the journal Psychological Science in the Public Interest (PSPI), however, reveals that even though a more extensive formal education forestalls the more obvious signs of age-related cognitive deficits, it does not lessen the rate of aging-related cognitive declines. Instead, people who have gone further in school attain, on average, a higher level of cognitive function in early and middle adult adulthood, so the initial effects of cognitive aging are initially less obvious and the most severe impairments manifest later than they otherwise would have.
“The total amount of formal education that people receive is related to their average levels of cognitive functioning throughout adulthood,” said Elliot M. Tucker-Drob, a researcher with the University of Texas, Austin, and coauthor on the paper. “However, it is not appreciably related to their rates of aging-related cognitive declines.”Continue reading →