In recent years, subcortical small-vessel disease has become an increasingly common cognitive diagnosis. Researchers at University of Gothenburg have now shown that it is possible to identify patients with the disease by combining two biomarkers that are measured in spinal fluid and blood, increasing the potential for both treatment and development of medication.
Subcortical small-vessel disease is one of the most common cognitive diseases, along with Alzheimer’s disease and mixed dementia, which is a form in which Alzheimer’s disease occurs together with vascular damage in the brain.
It’s long been believed that advancing age leads to broad declines in our mental abilities. Now, new research from Georgetown University Medical Center offers surprisingly good news by countering this view.
The findings, published August 19, 2021, in Nature Human Behavior, show that two key brain functions, which allow us to attend to new information and to focus on what’s important in a given situation, can in fact improve in older individuals. These functions underlie critical aspects of cognition such as memory, decision making, and self-control, and even navigation, math, language and reading.
Cognitive decline is the biggest factor in determining how long patients with Alzheimer’s Disease will live after being diagnosed, according to a new study from researchers at UT Southwestern. The findings, published in the Journal of Alzheimer’s Disease, are a first step that could help health care providers provide reliable prediction and planning assistance for patients with Alzheimer’s disease and their families.
Using a National Alzheimer’s Coordinating Center dataset on 764 autopsy-confirmed cases, C. Munro Cullum, Ph.D., Professor of Psychiatry, Neurology, and Neurological Surgery, and first author Jeffrey Schaffert, Ph.D., a postdoctoral fellow in clinical neuropsychology at UT Southwestern, identified seven factors that helped predict life expectancy variances among participants. These factors are the most predictive of how many years of life remain after diagnosis.
Daytime napping among older people is a normal part of aging – but it may also foreshadow Alzheimer’s disease and other dementias. And once dementia or its usual precursor, mild cognitive impairment, are diagnosed, the frequency and/or duration of napping accelerates rapidly, according to a new study.
The study, led by UC San Francisco, and Harvard Medical School together with Brigham and Women’s Hospital, its teaching affiliate, departs from the theory that daytime napping in older people serves merely to compensate for poor nighttime sleep. Instead, it points to work by other UCSF researchers suggesting that dementia may affect the wake-promoting neurons in key areas of the brain, the researchers state in their paper publishing March 17 in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association.
“We found the association between excessive daytime napping and dementia remained after adjusting for nighttime quantity and quality of sleep,” said co-senior author Yue Leng, MD, PhD, of the UCSF Department of Psychiatry and Behavioral Sciences.
“This suggested that the role of daytime napping is important itself and is independent of nighttime sleep,” said Leng, who partnered with Kun Hu, PhD, of Harvard Medical School, in senior-authoring the paper.
Watch-Like Devices, Annual Evaluations Used to Measure Naps, Cognition
In the study, the researchers tracked data from 1,401 seniors, who had been followed for up to 14 years by the Rush Memory and Aging Project at the Rush Alzheimer’s Disease Center in Chicago. The participants, whose average age was 81 and of whom approximately three-quarters were female, wore a watch-like device that tracked mobility. Each prolonged period of non-activity from 9 a.m. to 7 p.m. was interpreted as a nap.
Mental speed – the speed at which we can deal with issues requiring rapid decision-making – does not change substantially over decades. Psychologists at Heidelberg University have come to this conclusion. Under the leadership of Dr Mischa von Krause and Dr Stefan Radev, they evaluated data from a large-scale online experiment with over a million participants. The findings of the new study suggest that the speed of cognitive information processing remains largely stable between the ages of 20 and 60, and only deteriorates at higher ages. The Heidelberg researchers have hereby called into question the assumption to date that mental speed starts to decline already in early adulthood.
“The common assumption is that the older we get, the more slowly we react to external stimuli. If that were so, mental speed would be fastest at the age of about twenty and would then decline with increasing age,” says Dr von Krause, a researcher in the Quantitative Research Methods department headed by Prof. Dr Andreas Voß at Heidelberg University’s Institute of Psychology. In order to verify this theory, the researchers re-evaluated data from a large-scale American study on implicit biases. In the online experiment with over a million participants, subjects had to press a button to sort pictures of people into the categories “white” or “black” and words into the categories “good” or “bad”. According to Dr von Krause, the content focus was of minor importance in the Heidelberg study. Instead, the researchers used the large batch of data as an example of a response-time task to measure the duration of cognitive decisions.
Younger adults (ages 20-40) with high blood pressure had brain changes by midlife (average age 55) that may increase their risk of cognitive decline later in life or over time.
These changes were similar across all races and ethnic groups examined in the study when accounting for the degree of high blood pressure exposure.
The findings suggest health care professionals consider more aggressive high blood pressure treatment for younger adults to prevent brain changes in later life.
High blood pressure among younger adults, ages 20-40 years, appears to be linked to brain changes in midlife (average age 55) that may increase risk for later cognitive decline, according to preliminary research to be presented at the American Stroke Association’s International Stroke Conference 2022, a world premier meeting for researchers and clinicians dedicated to the science of stroke and brain health to be held in person in New Orleans and virtually, Feb. 8-11, 2022.
Good news for those of us who can’t face the day without their morning flat white: a long-term study has revealed drinking higher amounts of coffee may make you less likely to develop Alzheimer’s disease.
As part of the Australian Imaging, Biomarkers and Lifestyle Study of ageing, researchers from Edith Cowan University (ECU) investigated whether coffee intake affected the rate of cognitive decline of more than 200 Australians over a decade.
Lead investigator Dr. Samantha Gardener said results showed an association between coffee and several important markers related to Alzheimer’s disease.
“We found participants with no memory impairments and with higher coffee consumption at the start of the study had lower risk of transitioning to mild cognitive impairment — which often precedes Alzheimer’s disease — or developing Alzheimer’s disease over the course of the study,” she said.
As a senior citizen one of my most serious concerns is my mental functioning. My mother and her sister were afflicted with forms of dementia, including Alzheimer’s Disease. Also, my father’s father suffered cognitive problems in the 1940’s. Finally, my father’s sister and her daughter, my cousin had forms of dementia. It runs in my family and judging by the number of cases reported, there is a chance it runs in yours, too.
Here is what Alzheimers.gov has to say on the subject:
Alzheimer’s disease is a brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. People with Alzheimer’s also experience changes in behavior and personality.
More than 6 million Americans, many of them age 65 and older, are estimated to have Alzheimer’s disease. That’s more individuals living with Alzheimer’s disease than the population of a large American city. Many more people experience Alzheimer’s in their lives as family members and friends of those with the disease.
The symptoms of Alzheimer’s disease — changes in thinking, remembering, reasoning, and behavior — are known as dementia. That’s why Alzheimer’s is sometimes referred to as “dementia.” Other diseases and conditions can also cause dementia, with Alzheimer’s being the most common cause of dementia in older adults.
Alzheimer’s disease is not a normal part of aging. It’s the result of complex changes in the brain that start years before symptoms appear and lead to the loss of brain cells and their connections.
What Causes Alzheimer’s?
The causes of Alzheimer’s disease are not yet fully understood, but probably include a combination of:
Age-related changes in the brain, like shrinking, inflammation, blood vessel damage, and breakdown of energy within cells, which may harm neurons and affect other brain cells.
Changes or differences in genes, which may be passed down by a family member. Both types of Alzheimer’s — the very rare early-onset type occurring between age 30 and mid-60s, and the most common late-onset type occurring after a person’s mid-60s — can be related to a person’s genes in some way. Many people with Down syndrome, a genetic condition, will develop Alzheimer’s as they age and may begin to show symptoms in their 40s.
Health, environmental, and lifestyle factors that may play a role, such as exposure to pollutants, heart disease, stroke, high blood pressure, diabetes, and obesity.
Your dad just asked the same question he asked — and you answered — a few minutes ago. You realize that it’s not the first time he’s repeated himself or forgotten something you just said. What does this mean? Does he have Alzheimer’s disease?
Memory changes can be scary, both as an older adult experiencing them and as a family member or caregiver noticing them. But it’s important to note that forgetfulness doesn’t necessarily equal Alzheimer’s disease.
“The red flag is if it’s happening on a consistent basis and is paired with a change in the person’s ability to function,” says Magdalena Bednarczyk, MD, a geriatrician at Rush University Medical Center. “When a patient comes to me for an evaluation, it’s usually because family and friends have noticed uncharacteristic or concerning behaviors, not just memory issues.”
According to Bednarczyk and the Alzheimer’s Association, if you notice any of these 10 signs — especially more than one — talk to your loved one about seeing their primary care doctor or geriatrician as soon as possible:
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.”