Too much or too little sleep may increase dementia risk

By Brian P. Dunleavy

Getting too much or too little sleep may increase the risk for cognitive decline, or dementia, in older adults, according to a study published Monday by JAMA Network Open.

In an analysis of the sleep habits of more than 20,000 English and Chinese adults age 48 to 75, people who slept for fewer than four hours or more than 10 hours per day showed evidence of declines in cognitive function, including memory and language comprehension, researchers said.

“This study is an observational study and cannot demonstrate a causal relationship,” study co-author Yanjun Ma told UPI, so the findings don’t necessarily prove that lack of sleep or excessive sleep causes a decline in cognitive function.

Observational studies are intended to assess only the effect of an intervention — in this case, sleep — on study participants, without trying to modify it to compare differences.

It’s possible that diminished or excessive sleep is an early sign of cognitive decline or dementia, as opposed to a risk factor, researchers said.

“Future mechanism studies, as well as intervention studies examining the association between sleep duration and cognitive decline are required,” said Ma, of the Peking University Clinical Research Institute in China.

As many as 6 million Americans have some form of dementia, and changes in sleep patterns are common, according to the Alzheimer’s Association.

To date, research has shown that sleep disturbances can result from cognitive impairment, while animal studies have found links between lack of sleep and increased levels of brain proteins that are thought to be signs for Alzheimer’s disease, said Dr. Yue Leng, who authored a commentary on the study findings.

Leng is an assistant professor of psychiatry at the University of California-San Francisco.

For their research, Ma and colleagues analyzed data on sleep behaviors and cognitive function in 20,065 adults from the English Longitudinal Study of Aging and the China Health and Retirement Longitudinal Study, and tracked them for about eight years, on average.

In addition to finding higher levels of cognitive decline among those who slept fewer than four or more than 10 hours per day, the researchers also observed that people with these sleep habits had “faster cognitive decline” than those who slept seven to nine hours per day, Ma said.

“It’s usually believed that sleep deprivation might lead to cognitive decline, but it’s unclear why too much sleep might be bad for cognitive health,” Leng added. “Older adults should pay more attention to their sleep habits, as these might have implications for their cognitive health.”

https://www.upi.com/Health_News/2020/09/21/Too-much-or-too-little-sleep-may-increase-dementia-risk/5341600697569/

Playing video games in childhood improves working memory years later

By Chrissy Sexton

Playing video games as a child leads to long-lasting cognitive benefits, according to new research from the Universitat Oberta de Catalunya (UOC). The study suggests that gaming improves working memory and concentration.

Previous studies have shown that gaming improves attention, enhances visual-spatial skills, and causes structural changes in the brain – even increasing the size of some regions. The current study is the first to show that video games promote positive cognitive changes that can take place years after people stop playing them.

“People who were avid gamers before adolescence, despite no longer playing, performed better with the working memory tasks, which require mentally holding and manipulating information to get a result,” said study lead author Dr. Marc Palaus.

The research was focused on 27 people between the ages of 18 and 40 with and without any kind of video gaming experience.

The experts analyzed cognitive skills, including working memory, at three points during the study period: before training the volunteers to play Nintendo’s Super Mario 64, at the end of the training, and fifteen days later.

The findings revealed that participants who had not played video games in childhood did not benefit from improvements in processing and inhibiting irrelevant stimuli. As expected, these individuals were initially slower than those who had played games as children.

“People who played regularly as children performed better from the outset in processing 3D objects, although these differences were mitigated after the period of training in video gaming, when both groups showed similar levels,” said Dr. Palaus.

The experts also performed 10 sessions of a non-invasive brain stimulation known as transcranial magnetic stimulation on the individuals.

“It uses magnetic waves which, when applied to the surface of the skull, are able to produce electrical currents in underlying neural populations and modify their activity,” explained Palaus.

The researchers theorized that combining video gaming with this type of stimulation could improve cognitive performance, but that was not the case.

“We aimed to achieve lasting changes. Under normal circumstances, the effects of this stimulation can last from milliseconds to tens of minutes. We wanted to achieve improved performance of certain brain functions that lasted longer than this.”

The game used in the study had a 3D platform, but there are many types of video games that can influence cognitive functions. According to Dr. Palaus, what most video games have in common is that they involve elements that make people want to continue playing, and that they gradually get harder and present a constant challenge.

“These two things are enough to make it an attractive and motivating activity, which, in turn, requires constant and intense use of our brain’s resources,” said Dr. Palaus. “Video games are a perfect recipe for strengthening our cognitive skills, almost without our noticing.”

The study is published in the journal Frontiers in Human Neuroscience.

Playing video games in childhood improves working memory years later

Poor Sleep Linked with Future Amyloid-β Build Up

by Abby Olena

There’s evidence in people and animals that short-term sleep deprivation can change the levels of amyloid-β, a peptide that can accumulate in the aging brain and cause Alzheimer’s disease. Scientists now show long-term consequences may also result from sustained poor sleep. In a study published September 3 in Current Biology, researchers found that healthy individuals with lower-quality sleep were more likely to have amyloid-β accumulation in the brain years later. The study could not say whether poor sleep caused amyloid-β accumulation or vice versa, but the authors say that sleep could be an indicator of present and future amyloid-β levels.

“Traditionally, sleep disruptions have been accepted as a symptom of Alzheimer’s disease,” says Ksenia Kastanenka, a neuroscientist at Massachusetts General Hospital who was not involved in the work. Her group showed in 2017 that improving sleep in a mouse model of Alzheimer’s disease, in which the animals’ slow wave sleep is disrupted as it usually is in people with the disease, halted disease progression.

Collectively, the results from these studies and others raise the possibility that “sleep rhythm disruptions are not an artifact of disease progression, but actually are active contributors, if not a cause,” she says, hinting at the prospect of using these sleep measures as a biomarker for Alzheimer’s disease.

As a graduate student at the University of California, Berkeley, Joseph Winer, who is now a postdoc at Stanford University, and his colleagues were interested in whether or not sleep could predict how the brain changes over time. They collaborated with the team behind the Berkeley Aging Cohort Study, which includes a group of 32 cognitively healthy adults averaging about 75 years of age. They participated in a sleep study, then had periodic cognitive assessments and between two and five positron emission tomography (PET) scans to check for the presence of amyloid-β in their brains for an average of about four years after the sleep study.

The researchers found at their baseline PET scan, which happened within six months of their sleep study, that 20 of the 32 participants already had some amyloid-β accumulation, which was not unexpected based on their average age. They also showed that both slow wave sleep, an indicator of depth of sleep, and sleep efficiency, the amount of time sleeping compared to time in bed, were both predictive of the rate of amyloid change several years later. In other words, people with lower levels of slow wave sleep and sleep efficiency were more likely to have faster amyloid build up.

The subjects all remained cognitively healthy over the duration of the study, says Winer. “We do expect that they’re at higher risk for developing Alzheimer’s in their lifetime because of the amyloid plaque.”

The strengths of the study include the well-characterized participants with detailed sleep assessments, as well as cognitive testing and longitudinal amyloid PET imaging, says Brendan Lucey, a sleep neurologist at Washington University in St. Louis who did not participate in the work.

There are still open questions about the link between sleep and amyloid deposition over time. “Amyloid accumulation on PET increases at different rates in amyloid-negative and amyloid-positive individuals, and even within amyloid-positive individuals,” Lucey explains. “Without adjusting for participants’ starting amyloid [levels], we don’t know if some participants would have been more likely to have increased amyloid compared to others, independent of sleep.”

“It is very hard to untangle this question of baselines,” acknowledges Winer. Because the sleep measures the team identified in the study are related to amyloid levels, to actually tease apart the effect of sleep quality on amyloid deposition and vice versa, it’d be necessary to study people starting as early as their fifties, when they’re much less likely to have amyloid accumulation, he says.

This study is “a great start,” David Holtzman, a neurologist and collaborator of Lucey at Washington University in St. Louis who did not participate in the work, tells The Scientist. In addition to controlling for the amount of amyloid deposition that is present in a subject’s brain at the beginning of the study, it would be important to see if the findings bear out in larger numbers of people and what role genetic factors play.

“The most important question down the road is to test the idea in some sort of a treatment paradigm,” Holtzman adds. “You can do something to improve the quality of sleep or increase slow wave sleep, and then determine if it actually slows down the onset of Alzheimer’s disease clinically.”

J.R. Winer et al., “Sleep disturbance forecasts β-amyloid accumulation across subsequent years,” Current Biology, doi:10.1016/j.cub.2020.08.017, 2020.

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Long-term usage of antidepressant medications may protect from dementia

Long-term treatment with certain antidepressants appeared associated with reduced dementia incidence, according to results of a case-control study published in Journal of Clinical Psychiatry.

“Depression could represent one of these potentially modifiable risk factors for all-cause dementia,” Claudia Bartels, PhD, of the department of psychiatry and psychotherapy at University Medical Center Goettingen in Germany, and colleagues wrote. “Numerous studies have concordantly demonstrated a strong association between depression and an increased risk [for] subsequent dementia. Selective serotonin reuptake inhibitors (SSRIs) are commonly used to treat depressive symptoms in [Alzheimer’s disease] dementia.

“Preclinical research in recent years has suggested that SSRIs reduce amyloid plaque burden in transgenic mouse models of [Alzheimer’s disease] and in cognitively healthy humans, attenuate amyloid-[beta]1-42–induced tau hyperphosphorylation in cell culture and improve cognition in mice.”

However, the effects of SSRIs on cognition in Alzheimer’s disease dementia were linked mostly to negative results in randomized clinical trials; research is sparse regarding which antidepressants may influence risk for developing dementia; and evidence is particularly rare for treatment duration effects on this risk. Thus, Bartels and colleagues sought to determine the effects of antidepressant drug classes and individual compounds with various treatment durations on the risk for developing dementia. The researchers analyzed data of 62,317 individuals with an incident dementia diagnosis who were included in the German Disease Analyzer database, and they compared outcomes to those of controls matched by age, sex and physician. They conducted logistic regression analyses, which were adjusted for health insurance status and comorbid diseases linked to dementia or antidepressant use, to evaluate the association between dementia incidence and treatment with four major classes of antidepressant drug, as well as 14 of the most commonly prescribed individual antidepressants.

Results showed an association between treatment for 2 years or longer with any antidepressant and a lower risk for dementia vs. short-term treatment among 17 of 18 comparison. Particularly for long-term treatment, herbal and tricyclic antidepressants were linked to a decrease in incidence of dementia. Long-term treatment with escitalopram (OR = 0.66; 95% CI, 0.5-0.89) and Hypericum perforatum (OR = 0.6; 95% CI, 0.51-0.7) were associated with the lowest risks for dementia on an individual antidepressant basis.

“Clinical trials — although well acknowledged as the gold standard procedure — have debunked numerous promising compounds and become increasingly challenging with longer treatment durations,” Bartels and colleagues wrote. “Thus, and in awareness of the controversy of this suggestion, analyzing data from registries in a naturalistic setting may be an attractive and feasible alternative. If individual datasets could be combined in a multinational effort, even more powerful analyses of merged big databases could be performed and an additive contribution with naturalistic data could be made.”

https://www.healio.com/news/psychiatry/20200828/longterm-treatment-with-certain-antidepressants-may-reduce-dementia-incidence

Alzheimer’s risk factors may be measurable in adolescents and young adults

Risk factors for Alzheimer’s dementia may be apparent as early as our teens and 20s, according to new research reported at the Alzheimer’s Association International Conference® (AAIC®) 2020.

These risk factors, many of which are disproportionately apparent in African Americans, include heart health factors — such as high blood pressure, high cholesterol and diabetes — and social factors like education quality. According to the Alzheimer’s Association Alzheimer’s Disease Facts and Figures report, older African Americans are about twice as likely to have Alzheimer’s or other dementias as older whites.

“By identifying, verifying, and acting to counter those Alzheimer’s risk factors that we can change, we may reduce new cases and eventually the total number of people with Alzheimer’s and other dementia,” said Maria C. Carrillo, Ph.D., Alzheimer’s Association chief science officer. “Research like this is important in addressing health inequities and providing resources that could make a positive impact on a person’s life.”

“These new reports from AAIC 2020 show that it’s never too early, or too late, to take action to protect your memory and thinking abilities,” Carrillo said.

The Alzheimer’s Association is leading the U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (U.S. POINTER), a two-year clinical trial to evaluate whether lifestyle interventions that simultaneously target many risk factors protect cognitive function in older adults who are at increased risk for cognitive decline. U.S. POINTER is the first such study to be conducted in a large, diverse group of Americans across the United States.

African American Youth At Higher Risk of Dementia

In a population of more than 714 African Americans in the Study of Healthy Aging in African Americans (STAR), Kristen George, Ph.D., MPH, of the University of California, Davis, and colleagues found that high blood pressure and diabetes, or a combination of multiple heart health-related factors, are common in adolescence and are associated with worse late-life cognition. Study participants were adolescents (n=165; ages 12-20), young adults (n=439; ages 21-34) and adults (n=110; ages 35-56). Mean age at cognitive assessment was 68.

Cognition was measured using in-person tests of memory and executive function. The researchers found that, in this study population, having diabetes, high blood pressure, or two or more heart health risk factors in adolescence, young adulthood, or mid-life was associated with statistically significantly worse late-life cognition. These differences persisted after accounting for age, gender, years since risk factors were measured, and education.

Before this report, little was known about whether cardiovascular disease (CVD) risk factors developed prior to mid-life were associated with late-life cognition. This is an important question because African Americans have a higher risk of CVD risk factors compared to other racial/ethnic groups from adolescence through adulthood.

According to the researchers, these findings suggest that CVD risk factors as early as adolescence influence late-life brain health in African Americans. Efforts to promote heart and brain healthy lifestyles must not only include middle-aged adults, but also younger adults and adolescents who may be especially susceptible to the negative impact of poor vascular health on the brain.

Early Adult BMI Associated With Late Life Dementia Risk

In what the authors say is the first study to report on the issue, higher early adulthood (age 20-49) body mass index (BMI) was associated with higher late-life dementia risk.

Relatively little is known about the role of early life BMI on the risk of Alzheimer and other dementias. The scientists studied a total of 5,104 older adults from two studies, including 2,909 from the Cardiovascular Health Study (CHS) and 2,195 from the Health, Aging and Body Composition study (Health ABC). Of the total sample, 18% were Black and 56% were women. Using pooled data from four established cohorts spanning the adult life course, including the two cohorts under the study, the scientists estimated BMI beginning at age 20 for all older adults of CHS and Health ABC.

For women, dementia risk increased with higher early adulthood BMI. Compared to women with normal BMI in early adulthood, dementia risk was 1.8 times higher among those who were overweight, and 2.5 times higher among those who were obese. Analyses were adjusted for midlife and late life BMI.

They found no association between midlife BMI and dementia risk among women.

For men, dementia risk was 2.5 times higher among those who were obese in early adulthood, 1.5 times higher among those who were overweight in mid-life and 2.0 times higher among those who were obese in mid-life, in models also adjusted for late life BMI.

For both women and men, dementia risk decreased with higher late life BMI.

Adina Zeki Al Hazzouri, Ph.D. of Columbia University and colleagues found that high BMI in adulthood is a risk factor for dementia in late life. The researchers suggest that efforts aimed at reducing dementia risk may need to begin earlier in life with a focus on obesity prevention and treatment.

Quality of Early-Life Education Influences Dementia Risk

In a diverse group of more than 2,400 people followed up to 21 years, higher quality early-life education was associated with better language and memory performance, and lower risk of late-life dementia. Results were somewhat different between men and women, and between Blacks and Whites in the study.

The study included 2,446 Black and White men and women, age 65 and older, enrolled in the Washington Heights/Inwood Columbia Aging Project who attended elementary school in the United States. A school quality variable based on historical measures included: mandatory school enrollment age, minimum dropout age, school term length, student-teacher ratio, and student attendance.

People who attended school in states with lower quality education had more rapid decline in memory and language as an older adult. Black women and men and White women who attended schools in states with higher quality education were less likely to develop dementia. According to the scientists, the results were explained, in part, because people who attend higher quality schools end up getting more years of school.

Justina Avila-Rieger, PhD, a postdoctoral research scientist at Columbia University Irving Medical Center and colleagues say the findings provide evidence that later life dementia risk and cognitive function is influenced by early-life state educational policies.

https://www.sciencedaily.com/releases/2020/07/200730092616.htm

Experimental Blood Test Could Flag Alzheimer’s


New studies show that elevated levels of a form of tau called p-tau217 can accurately distinguish Alzheimer’s disease from other forms of dementia, and perhaps even predict it.

by Kerry Grens

Three studies presented at the Alzheimer’s Association International Conference this week describe the performance of blood tests used to diagnose, and even predict, Alzheimer’s disease using circulating levels of a form of tau protein called p-tau217. The largest assessment of this approach, which included 1,402 participants, showed that circulating p-tau217 levels worked just as well at detecting Alzheimer’s as standard PET scans and tests of cerebrospinal fluid.

“This blood test very, very accurately predicts who’s got Alzheimer’s disease in their brain, including people who seem to be normal,” Michael Weiner, an Alzheimer’s disease researcher at the University of California, San Francisco, who was not involved in the study, tells The New York Times. “It’s not a cure, it’s not a treatment, but you can’t treat the disease without being able to diagnose it. And accurate, low-cost diagnosis is really exciting, so it’s a breakthrough.”

A blood test could help identify people on track to develop Alzheimer’s early on—and perhaps get them enrolled in drug trials aimed at finding an effective treatment for the disease. Scientists have pursued a number of potential circulating biomarkers, such as amyloid-β, to find those that can reliably diagnose Alzheimer’s disease or predict its development, but to date none have come to market.

High levels of tau or its phosphorylated form, p-tau, have emerged as promising biomarker candidates because they may indicate the presence of damaging structures known as neurofibrillary tangles in the brain.

The large study on one type of p-tau, p-tau217, published in JAMA July 28 to coincide with the presentation at the meeting, was a collection of three experiments using a blood test developed by Eli Lilly (some of the coauthors work for the company). In one assessment of several hundred Swedes, the test accurately distinguished patients who had Alzheimer’s from those with other forms of dementia with 89–98 percent accuracy. “That’s pretty good. We’ve never seen that” precision before, Maria Carrillo, the Alzheimer’s Association’s chief science officer, tells the Associated Press.

In another assessment of the Eli Lilly test, which included hundreds of related individuals, some of whom have a gene that causes Alzheimer’s, p-tau217 levels in the blood aligned with the genetics, even decades before cognitive impairment is likely to begin.

Another study presented at the conference found a p-tau217 blood test could accurately distinguish Alzheimer’s patients from those with frontotemporal lobar degeneration, according to a conference press release. And a third presentation of a study by Suzanne Schindler of Washington University in St. Louis and her colleagues reported that circulating p-tau217 was superior to another form that’s been studied as a potential biomarker, p-tau181, as a proxy for amyloid accumulation in the brain.

“I personally find it very reassuring that these different groups are using different types of assays and getting the same result,” Schindler tells the Times. “It looks real. It looks like 217 has tremendous promise as a blood test for Alzheimer’s disease, and it is likely to correspond with the symptoms.”

Speaking to The Guardian, Clive Ballard, who studies age-related disease at the University of Exeter Medical School and who was not involved in these projects, says, “further validation in people from more routine clinical settings are still needed, and a lot of work will be needed to achieve standardisation of the test across laboratories—so it could still be at least five years before we see an accurate blood biomarker test for dementia in the clinic.”

https://www.the-scientist.com/news-opinion/experimental-blood-test-could-flag-alzheimers-67779?utm_campaign=TS_DAILY%20NEWSLETTER_2020&utm_medium=email&_hsmi=92321648&_hsenc=p2ANqtz-8ayk91AfO8kNKldfK3kfssyQf2GRuKPsOimQKjhl3hz5Ap-KFfFI0molaN5LwimzBJw9JHyX8TCowcon5V50G5hr5ErA&utm_content=92321648&utm_source=hs_email

Neupro may reduce cognitive dysfunction among patients with Alzheimer’s disease

The dopaminergic agonist Neupro appeared to improve frontal cognitive functions and activities of daily living among patients with mild to moderate Alzheimer’s disease, according to study results published in JAMA Network Open.

“Some early attempts have been carried out using dopaminergic drugs, such as L-dopa or selegiline, in samples of patients with Alzheimer’s disease at different stages of the disease, with some controversial results,” Giacomo Koch, MD, PhD, of the department of behavioral and clinical neurology at Santa Lucia Foundation Scientific Institute for Research, Hospitalization and Healthcare in Rome, and colleagues wrote. “More recently, experimental studies in animal models of Alzheimer’s disease showed that dopaminergic agonists may reduce amyloid deposition and improve memory and that the degeneration of dopaminergic neurons in the ventral tegmental area contributes to memory deficits. It has also been shown that in the early stages of Alzheimer’s disease, dopaminergic agonists improve cholinergic transmission and cortical plasticity likely by acting on the dopaminergic projections over the frontal cortex.”

This prior evidence suggested novel implications for therapies based on dopaminergic stimulation among patients with mild to moderate Alzheimer’s disease, according to the investigators. Thus, they sought to determine whether dopaminergic agonist therapy would affect cognitive functions among this patient population.

In the current phase 2, monocentric, randomized, double-blind, placebo-controlled trial conducted in Italy and funded by the Alzheimer’s Drug Discovery Foundation, Koch and colleagues enrolled 94 patients (mean age, 73.9 years) with mild to moderate Alzheimer’s disease between September 2017 and December 2018. The intervention comprised use of a Neupro (rotigotine, UCB) 2 mg transdermal patch for 1 week, followed by a 4 mg patch for 23 weeks among 47 patients or a placebo transdermal patch for 24 weeks among 47 patients. Change from baseline on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale served as the primary end point. Secondary end points included changes in Frontal Assessment Battery, Alzheimer’s Disease Cooperative Study-Activities of Daily Living and Neuropsychiatric Inventory scores. The researchers used transcranial magnetic stimulation combined with electroencephalography to evaluate prefrontal cortex activity.

A total of 78 patients completed the study. Results showed rotigotine compared with placebo had no significant effect on the primary end point, with an estimated mean change in Alzheimer’s Disease Assessment Scale-Cognitive Subscale score of 2.92 (95% CI, 2.51-3.33) among the rotigotine group and 2.66 (95% CI, 2.31-3.01) among the placebo group. The researchers reported significant estimated mean changes for the secondary outcomes between groups for Alzheimer Disease Cooperative Study-Activities of Daily Living score, which was 3.32 (95% CI, 4.02 to 2.62) among the rotigotine group and 7.24 (95% CI, 7.84 to 6.64) among the placebo group. Frontal Assessment Battery score was 0.48 (95% CI, 0.31-0.65) among the rotigotine group and 0.66 (95% CI, 0.80 to 0.52) among the placebo group. Koch and colleagues observed no longitudinal change in Neuropsychiatric Inventory scores for either group. Neurophysiological analysis of electroencephalography results revealed increased prefrontal cortical activity among the rotigotine group but not the placebo group. Patients in the rotigotine group were more likely to experience adverse events than the placebo group, and 11 patients dropped out compared with five, respectively.

“This study provides novel evidence that drugs acting on the dopaminergic system may be helpful to improve cognitive functions related to the frontal lobe activity,” Koch told Healio Psychiatry. “We hope that this research will expand Alzheimer’s disease therapy to drugs acting on different neurotransmission systems, such as the dopaminergic one, in addition to the cholinergic drugs.”

https://www.healio.com/news/psychiatry/20200715/neupro-may-reduce-cognitive-dysfunction-among-patients-with-alzheimers-disease?utm_source=ADDF&utm_campaign=e9d85ea654-EMAIL_CAMPAIGN_2019_11_18_10_21_COPY_01&utm_medium=email&utm_term=0_cc5f9da121-e9d85ea654-97060793

Higher BMI in early adulthood linked to increased dementia risk, new study suggests


Risk is 1.8 times higher for overweight women and 2.5 times higher for men

by Ella Pickover

People who are overweight in early adult life may be more prone to dementia in later life, a study suggests.

Those aged 20 to 49 who have a high body mass index have a higher risk of dementia later on, the authors said.

Researchers from Columbia University in the US studied data on more than 5,000 adults.

Compared with women who had a normal BMI, those who were overweight had a 1.8 times higher risk of dementia later on in life.

Obese women had a 2.5 times higher risk.

For men, dementia risk was 2.5 times higher among those who were obese in early adulthood, according to the findings presented to the Alzheimer’s Association International Conference.

An association was found between being overweight or obese in mid-life – classed in the study as people aged 50 to 69 – among men but not women.

Both men and women have a higher chance of dementia if they are obese in later life, the researchers found.

Commenting on the study, Dr Rosa Sancho, head of research at Alzheimer’s Research UK, said: “This study links a higher BMI in early adulthood with an increased risk of dementia later in life and underlines the importance of maintaining a healthy weight to help support a healthy brain.”

But more studies are needed to examine the link in more detail, she said, adding: “We know that diseases that cause dementia get under way in the brain many years before symptoms start to show. Studies looking at our lifestyle in early adulthood are important to help us build a picture of the factors that could impact our brain health as we age.”

Fiona Carragher, director of research and influencing at Alzheimer’s Society, added: “A healthy and balanced lifestyle is an important step towards reducing the risk of dementia later in life.

“Previous research we’ve supported, such as the 2017 Lancet commission, has shown that obesity in mid-life may increase dementia risk, so it’s interesting to see a study that shows this may also be the case in younger people too. But this can’t tell us if high BMI is a direct cause of dementia, there could be other factors at play.

“The number of people living with dementia is set to rise to one million by 2025 so it’s becoming increasingly urgent that we find ways to prevent people developing the condition in the first place.

“We can all take steps towards a healthy lifestyle, whether it’s by watching our diets or making the most of the sunny days and getting outside for a walk – it’s never too late, or early, to make a change.

“Research funding also plays a vital role here, hit badly by the current pandemic – so it’s critical that the government commits to their pledge to double life-saving research funding for the chronically under-funded field of dementia.”

https://www.independent.co.uk/news/uk/home-news/bmi-early-adulthood-increased-dementia-risk-us-a9645101.html

Aerobic exercise limits risk of Alzheimer’s in vulnerable adults


A new study has found a new link between regular aerobic exercise and improved cognitive function in brain regions associated with Alzheimer’s disease.

By Nick Lavars

Previous research has shown us how regular exercise can be beneficial for cognitive function and help stave off the brain degeneration associated with dementia and Alzheimer’s, but scientists continue to learn more about the mechanisms at play. The latest discovery in this area comes courtesy of researchers from the University of Wisconsin (UW), who have published a new study describing a relationship between regular aerobic exercise and a reduced vulnerability to Alzheimer’s among high-risk adults.

More and more research is establishing stronger and stronger links between exercise and the prevention or slowing of Alzheimer’s and dementia. Last September, one study found that a regime of regular aerobic exercise could slow the degeneration of the hippocampus, while another from early in 2019 found that a hormone released during exercise can improve brain plasticity and memory.

For the new study, the UW researchers enlisted 23 subjects, with the participants all cognitively healthy young adults but with a heightened risk of Alzheimer’s due to family history and genetics. All lived what the researchers describe as a sedentary lifestyle and were first put through examinations to assess their cardiorespiratory fitness, cognitive function, typical daily physical activity, and brain glucose metabolism, which is considered a measure of neuronal health.

From there, half of the subjects were given information about how to lead a more active lifestyle, but were then left to their own devices. The other half of the group was given a personal trainer and put through a treadmill training program described as “moderate intensity,” involving three sessions a week across 26 weeks.

Unsurprisingly, the active group demonstrated improved cardio fitness and took on less sedentary lifestyles once the training program had finished. But in addition, they scored higher on cognitive tests of executive functioning, which is the capacity of the brain to plan, pay attention, remember instructions and multitask. Executive function is known to deteriorate during the onset of Alzheimer’s.

“This study is a significant step toward developing an exercise prescription that protects the brain against AD, even among people who were previously sedentary,” explains lead investigator Ozioma C. Okonkwo.

In addition to this improved executive function, brain scans also revealed some marked differences in brain glucose metabolism in the posterior cingulate cortex, a region again linked with Alzheimer’s.

“This research shows that a lifestyle behavior – regular aerobic exercise – can potentially enhance brain and cognitive functions that are particularly sensitive to the disease,” says Okonkwo. “The findings are especially relevant to individuals who are at a higher risk due to family history or genetic predisposition.”

With the sample size on the small side, the researchers are now working towards larger studies with more subjects to see if their findings can be replicated.

The research was published in the journal Brain Plasticity.

https://newatlas.com/medical/aerobic-exercise-risk-alzheimers-vulnerable-adults/

Midlife Obesity in Women May Increase Risk for Dementia Later

In women, midlife obesity is associated with increased risk for dementia later in life, while no clear associations are apparent for low body mass index (BMI), low caloric intake, or inactivity at baseline, according to a study published online Dec. 18 in Neurology.

Sarah Floud, Ph.D., from the University of Edinburgh in the United Kingdom, and colleagues recruited 1,136,846 U.K. women (mean age, 56 years) in 1996 to 2001 and asked them about height, weight, caloric intake, and inactivity. The women were followed until 2017 by electronic linkage to National Health Service records.

Fifteen years after the baseline survey, 89 percent of participants remained alive with no detected dementia, 18,695 of whom had dementia detected later (mean age, 77 years). The researchers observed an association between dementia detection during years 15+ and baseline obesity (BMI, 30+ versus 20 to 24 kg/m² rate ratio, 1.21); no clear associations were seen with low BMI, low caloric intake, or inactivity at baseline. These three factors correlated with increased dementia rates during the first decade; over time, these correlations weakened considerably, approaching null after 15 years.

“In this population, midlife obesity is the only factor examined that is likely to be causally related to dementia, perhaps chiefly through its effects on vascular disease,” the authors write.

https://www.physiciansbriefing.com/neurology-9/dementia-news-738/midlife-obesity-in-women-may-increase-risk-for-dementia-later-753066.html