A study published in the Journal of the American Geriatrics Society found that immediately after retirement, white adults tended to experience a significant decline in cognitive function, whereas Black adults experienced minimal cognitive decline. White men showed the steepest post-retirement cognitive decline across sex/race combinations, whereas Black women showed the least decline.
White women performed better cognitively at retirement than other race/sex subgroups, and after retirement, their cognitive functioning declined at a rate that was slightly less than the average for this study. Results were adjusted for sociodemographics and physical and mental health indicators.
The study, which included 2226 US participants followed for up to 10 years, revealed greater post-retirement cognitive decline among individuals who attended college compared with those who did not.
“The results seem to point to the possibility that better job opportunities could lead to greater cognitive losses after retirement whereas exposure to lifelong structural inequalities may actually ease transition to retirement with respect to cognitive aging,” said lead author Ross Andel, PhD, of Arizona State University’s Edson College of Nursing and Health Innovation.
New research reveals that the level of muscle adiposity (fat content) may indicate a person’s likelihood of experiencing cognitive decline as they age. In the study published in the Journal of the American Geriatrics Society, a five-year increase in fat stored in the thigh muscle was a risk factor for cognitive decline.
This risk was independent of total weight, other fat deposits, and muscle characteristics (such as muscle strength or mass) and also independent of traditional dementia risk factors.
Investigators assessed muscle fat in 1634 adults 69–79 years of age at years 1 and 6 and evaluated their cognitive function at years 1, 3, 5, 8, and 10. Increases in muscle adiposity from year 1 to year 6 were associated with faster and more cognitive decline over time. The findings were similar for Black and White men and women.
“Our data suggest that muscle adiposity plays a unique role in cognitive decline, distinct from that of other types of fat or other muscle characteristics,” said corresponding author Caterina Rosano, MD, MPH, of the University of Pittsburgh’s School of Public Health. “If that is the case, then the next step is to understand how muscle fat and the brain ‘talk’ to each other, and whether reducing muscle adiposity can also reduce dementia risk.”
Low sexual satisfaction in middle age may serve as an early warning sign for future cognitive decline, according to a new study. The researchers, who tracked associations between erectile function, sexual satisfaction and cognition in hundreds of men aged 56 through 68, found that declines in sexual satisfaction and erectile function were correlated with future memory loss.
The study, published inGerontologist, is the first to longitudinally track sexual satisfaction in tandem with sexual health and cognition, the researchers state, and its findings point to a potential novel risk factor for cognitive decline.
“What was unique about our approach is that we measured memory function and sexual function at each point in the longitudinal study, so we could look at how they changed together over time,” said Martin Sliwinski, professor of human development and family studies at Penn State and co-author on the study. “What we found connects to what scientists are beginning to understand about the link between life satisfaction and cognitive performance.”
The study explored the relationship between physical changes like the microvascular changes relevant for erectile function, and psychological changes, such as lower sexual satisfaction, to determine how the changes relate to cognition. They examined the shifts starting in middle age because it represents a transition period where declines in erectile function, cognition and sexual satisfaction begin to emerge.
Sliwinski added that while the team discovered a strong correlation between the three health factors, they can only speculate as to the cause.
“Scientists have found that if you have low satisfaction generally, you are at a higher risk for health problems like dementia, Alzheimer’s disease, cardiovascular disease and other stress-related issues that can lead to cognitive decline,” he said. “Improvements in sexual satisfaction may actually spark improvement in memory function. We tell people they should get more exercise and eat better foods. We’re showing that sexual satisfaction also has importance for our health and general quality of life.”
For the study, the researchers used survey data from 818 men who participated in the Vietnam Era Twin Study of Aging. Through neuropsychological tests, such as tests of memory and processing speed, they examined cognitive changes of participants over the 12-year span from age 56 to 68, adjusting for participants’ cognitive ability in young adulthood. Their erectile function and sexual satisfaction were measured alongside cognition, using the International Index of Erectile Function, a self-reported assessment for male sexual health. The researchers then built a statistical model to understand how the three variables changed as individuals aged.
“Research on sexual health has historically focused on quantifiable facets of sexuality like number of sexual partners or frequency of sexual activity,” said Riki Slayday, a doctoral candidate at Penn State and lead author on the study. “What we were interested in is the perception of that activity, how someone feels about their sex life, and how that influences cognitive function, because multiple people could be in the same situation physically but experience completely different levels of satisfaction.”
The study found that decreases in erectile function and sexual satisfaction were both associated with memory decline, which the researchers say points to a connection between psychological and physical health.
“When we mapped the relationship over time, we found increases or decreases in erectile function and sexual satisfaction were associated with concurrent increases or decreases in cognitive function,” Slayday said. “These associations survived adjustment for demographic and health factors, which tells us there is a clear connection between our sex lives and our cognition.”
Prior studies have found a link between microvascular changes and changes in erectile function over time. In fact, the active ingredient in Viagra (Sildenafil) was originally developed to treat cardiovascular problems, Sliwinski explained, so the connection between vascular health and erectile function is well understood. How erectile function connects to other aspects of health should be an area of focus for future research, he added.
Increasing the assessment and monitoring of erectile function as a vital sign of health may help identify those at risk of cognitive decline before their 70s, he said. The researchers note that the older adult population in the US is expected to double over the next 30 years, which means twice as many people will likely enter their 60s and experience declines in erectile function and sexual satisfaction.
“We already have a pill for treating erectile dysfunction. What we don’t have is an effective treatment for memory loss,” Sliwinski said. “Instead of the conversation being about treating ED, we should see that as a leading indicator for other health problems and also focus on improving sexual satisfaction and overall well-being, not just treating the symptom.”
Adding to the growing body of evidence on sleep disturbances and cognitive impairment, new research published in the American Journal of Preventive Medicine, finds significant links between three measures of sleep disturbance and the risk for developing dementia over a 10-year period. Difficulties falling asleep were linked to higher risk, but not falling asleep again after waking.
The results associate sleep-initiation insomnia (trouble falling asleep within 30 min) and sleep medication use with higher dementia risk. An additional, surprising finding was that people who reported having sleep-maintenance insomnia (trouble falling back to sleep after waking) were less likely to develop dementia over the course of the study.
“We expected sleep-initiation insomnia and sleep medication usage to increase dementia risk, but we were surprised to find sleep-maintenance insomnia decreased dementia risk,” explained lead investigator Roger Wong, PhD, MPH, MSW, an Assistant Professor in the Department of Public Health and Preventive Medicine, SUNY Upstate Medical University. “The motivation behind this research was prompted on a personal level. My father has been experiencing chronic sleep disturbances since the COVID pandemic began, and I was concerned how this would affect his cognition in the future. After reading the existing literature, I was surprised to see mixed findings on the sleep-dementia relationship, so I decided to investigate this topic.”
This research is novel because it is the first to examine how long-term sleep disturbance measures are associated with dementia risk using a nationally representative US older adult sample. Previous research has associated REM sleep behavior, sleep deprivation (less than five hours of sleep), and the use of short-acting benzodiazepines with cognitive decline. Their results for sleep-maintenance insomnia support other recent studies using smaller, separate data samples.
This study used 10 annual waves (2011–2020) of prospective data from the National Health and Aging Trends Study (NHATS), a longitudinal panel study that surveys a nationally representative sample of Medicare beneficiaries aged 65 years and older within the USA. This study included only people who were dementia-free at baseline in 2011.
While the mechanism for decreased dementia risk among those with sleep-maintenance insomnia is still unknown, the investigators theorise that greater engagement in activities that preserve or increase cognitive reserve may thereby decrease dementia risk.
Recent evidence indicates there is a higher prevalence of sleep disturbances among older adults than among other age groups. This could be attributed to a variety of factors including anxiety about the COVID pandemic or warmer nights as a consequence of climate change.
“Older adults are losing sleep over a wide variety of concerns. More research is needed to better understand its causes and manifestations and limit the long-term consequences,” added Dr Wong. “Our findings highlight the importance of considering sleep disturbance history when assessing the dementia risk profile for older adults. Future research is needed to examine other sleep disturbance measures using a national longitudinal sample, whether these sleep-dementia findings hold true for specific dementia subtypes, and how certain sociodemographic characteristics may interact with sleep disturbances to influence dementia risk.”
Canadian and UK researchers explored the relationship between vitamin D supplementation and dementia in more than 12 388 participants of the US National Alzheimer’s Coordinating Center, who had a mean age of 71 and were dementia-free when they signed up.
The team found that taking vitamin D was associated with living dementia-free for longer, and they also found 40% fewer dementia diagnoses in the group who took supplements.
Of the group, 2696 participants progressed to dementia over ten years; amongst them, 2017 (75%) had no exposure to vitamin D throughout all visits prior to dementia diagnosis, and 679 (25%) had baseline exposure.
Professor Zahinoor Ismail, of the University of Calgary and University of Exeter, who led the research, said: “We know that vitamin D has some effects in the brain that could have implications for reducing dementia, however so far, research has yielded conflicting results. Our findings give key insights into groups who might be specifically targeted for vitamin D supplementation. Overall, we found evidence to suggest that earlier supplementation might be particularly beneficial, before the onset of cognitive decline.”
While Vitamin D was effective in all groups, the team found that effects were significantly greater in females, compared to males. Similarly, effects were greater in people with normal cognition, compared to those who reported signs of mild cognitive impairment – changes to cognition which have been linked to a higher risk of dementia.
The effects of vitamin D were also significantly greater in people who did not carry the APOEe4 gene, known to present a higher risk for Alzheimer’s dementia, compared to non-carriers. The authors suggest that people who carry the APOEe4 gene absorb vitamin D better from their intestine, which might reduce the vitamin D supplementation effect. However, no blood levels were drawn to test this hypothesis.
Previous research has found that low levels of vitamin D are linked to higher dementia risk. Vitamin D is involved in the clearance of amyloid in the brain, the accumulation of which is one of the hallmarks of Alzheimer’s disease. Studies have also found that vitamin D may provide help to protect the brain against build-up of tau, another protein involved in the development of dementia.
Co-author Dr Byron Creese, at the University of Exeter, said: “Preventing dementia or even delaying its onset is vitally important given the growing numbers of people affected. The link with vitamin D in this study suggests that taking vitamin D supplements may be beneficial in preventing or delaying dementia, but we now need clinical trials to confirm whether this is really the case. The ongoing VitaMIND study at the University of Exeter is exploring this issue further by randomly assigning participants to either take vitamin D or placebo and examining changes in memory and thinking tests over time.”
Scientists have developed a variety of games designed to boost older adults’ cognitive capacity. Co-creator Professor Adam Gazzaley, MD, PhD, said the games can be an “experiential medicine”. The games adapt to the players’ skill on the fly, and were shown to confer benefits on many important cognitive processes such as short-term memory, attention and long-term memory.
Each game uses adaptive closed-loop algorithms that Dr Gazzaley’s lab pioneered in the widely cited 2013 Neuroracer study published in Nature, which first demonstrated it was possible to restore diminished mental faculties in older people with just four weeks of training on a specially designed video game. The most recent game, which uses drumming, is described in in PNAS.
These algorithms get better results than commercial games by automatically adjusting in difficulty according to the players’ skills. The games using these algorithms recreate common activities, such as driving, exercising and playing a drum, and use the skills each can engender to retrain cognitive processes that decline with age.
“All of these are taking experiences and delivering them in a very personalised, fun manner, and our brains respond through a process called plasticity,” said Prof Gazzaley at the UCSF Weill Institute for Neurosciences and who is founder and executive director of Neuroscape. “Experiences are a powerful way of changing our brain, and this form of experience allows us to deliver it in a manner that’s very accessible.”
The lab’s most recent invention is a musical rhythm game, developed in consultation with drummer Mickey Hart, that not only taught the 60 to 79-year-old participants how to drum, but also improved their ability to remember faces.
The eight-week program used visual cues to train people how to play a rhythm on an electronic tablet, with an algorithm matching difficulty to the player’s ability. The cues disappeared over time, forcing the players to memorise the rhythmic pattern.
When the participants were tested at the end to see how well they could recognise unfamiliar faces, electroencephalography (EEG) data showed increased activity in a part of the brain on the right side (the superior parietal lobule) that is involved both in sight reading music and in short-term visual memory for other tasks. The researchers said the data indicate that the training improved how people bring something into memory and then take it back out again when they need it.
A second game, the Body Brain Trainer, published recently in NPJ Aging, improved blood pressure, balance and attention in a group of healthy older adults with eight weeks of training, as well as a key signature of attention that declines with age. The game also included a feedback mechanism.
“We had people wearing a heart rate monitor, and we were getting that heart rate data and feeding it into the game,” said Joaquin A. Anguera, PhD, associate professor of neurology at UCSF and director of the Clinical Division at Neuroscape. “If they weren’t working hard enough, the game got harder.”
Neuroscape published the results of a third study last year in Scientific Reports on a virtual reality spatial navigation game called Labyrinth that improved long-term memory in older adults after four weeks of training.
“These are all targeting cognitive control, an ability that is deficient in older adults and that is critical for their quality of life,” Prof Gazzaley said. “These games all have the same underlying adaptive algorithms and approach, but they are using very, very different types of activity. And in all of them we show that you can improve cognitive abilities in this population.”
A major analysis of all relevant published studies indicates that poor periodontal health and tooth loss may increase the risk of both cognitive decline and dementia. The finding, published in the Journal of the American Geriatrics Society, affirms a long-suspected connection between dental and cognitive health.
The analysis included 47 studies. Poor periodontal health, reflected by having periodontitis, tooth loss, deep periodontal pockets, or alveolar bone loss, was linked to a 23% increase in risk for cognitive decline and a 21% higher risk of dementia. Tooth loss on its own was associated with a 23% higher odds of cognitive decline and a 13% higher risk of dementia. The overall quality of evidence was low, however.
“From a clinical perspective, our findings emphasise the importance of monitoring and management of periodontal health in the context of dementia prevention, although available evidence is not yet sufficient to point out clear ways for early identification of at-risk individuals, and the most efficient measures to prevent cognitive deterioration,” the authors wrote.
A study published in Metabolic Brain Disease has established a clear link between mice being fed a high-fat diet for 30 weeks, resulting in diabetes, and a subsequent worsening of their cognitive abilities. This included developing anxiety, depression and worsening Alzheimer’s disease.
Mice with impaired cognitive function were also more likely to gain excessive weight due to poor metabolism caused by brain changes.
Neuroscientist and biochemist Associate Professor Larisa Bobrovskaya, who co-led the study said that the research adds to the growing body of evidence linking chronic obesity and diabetes with Alzheimer’s disease.
“Obesity and diabetes impair the central nervous system, exacerbating psychiatric disorders and cognitive decline. We demonstrated this in our study with mice,” said Associate Prof Bobrovskaya.
In the study, mice were randomised to a standard diet or a high-fat diet for 30 weeks, starting at eight weeks of age. Food intake, body weight and glucose levels were monitored at different intervals, along with glucose and insulin tolerance tests and cognitive dysfunction.
The mice on the high-fat diet gained significant weight, developed insulin resistance and started behaving abnormally compared to those fed a standard diet.
Genetically modified Alzheimer’s disease mice showed a significant deterioration of cognition and pathological changes in the brain while fed the high fat diet.
“Obese individuals have about a 55 per cent increased risk of developing depression, and diabetes will double that risk,” Assoc Prof Bobrovskaya said.
“Our findings underline the importance of addressing the global obesity epidemic. A combination of obesity, age and diabetes is very likely to lead to a decline in cognitive abilities, Alzheimer’s disease and other mental health disorders.”
Previous studies looking for an association between the neurodegenerative disorder glaucoma and cognitive function have produced mixed results. Now, findings from a large study recently published in the Journal of the American Geriatrics Society suggest that any association, if it exists, will only be small.
Glaucoma, the leading cause of irreversible blindness, is a progressive optic neuropathy with incompletely understood pathogenesis that results in progressive vision loss, often beginning with peripheral visual field defects.As a neurodegenerative process, glaucoma is associated with trans-synaptic degeneration in the brain, specifically in the lateral geniculate nucleus and visual cortex. Some prior studies have suggested that the pathogenesis of primary open angle glaucoma (POAG) and normal tension glaucoma (NTG), specifically, may be part of a broad neurodegenerative mechanism with ocular and non-ocular manifestations. Evidence also suggests that impaired vision is associated with a significant increase in the risk of accelerated cognitive decline and incident dementia. Therefore, there is interest in measuring an association between glaucoma and dementia.
The study included 7073 US adults aged 51 years and older who were interviewed by phone every two years. Those who developed glaucoma tended to have higher cognitive function scores but steeper rates of cognitive score decline over a maximum follow-up time of 18 years. The observed associations between glaucoma and cognitive function were small and unlikely to be clinically meaningful.
“In this large longitudinal study, a diagnosis of glaucoma was not associated with steeper rates of cognitive decline; however, this study did not have access to clinical data to determine whether glaucoma-related vision loss is a risk factor for cognitive decline and dementia,” said senior author Joshua R. Ehrlich MD, MP, of the University of Michigan Medical School. “This is an important question for future studies to consider.”
Researchers have found that quantifiable changes can be measured in dogs suspected of suffering from cognitive decline: an approach that could serve as a model for evaluating cognitive decline progression in, and treatments for, humans with Alzheimer’s disease.
In dogs there is a similar condition to similar to Alzheimer’s disease in humans, canine cognitive dysfunction syndrome (CCDS). In CCDS, cognitive decline is associated with the development of amyloid plaques as well as cortical atrophy. CCDS is also challenging to diagnose. Traditionally, CCDS is diagnosed based on ruling out any obvious physical conditions and an owner’s answers to a questionnaire.
“One problem with the current approach is that questionnaires only capture a constellation of home behaviours,” explained Professor Natasha Olby, co-senior author of the paper. “There can be other reasons for what an owner may perceive as cognitive decline – anything from an undiagnosed infection to a brain tumour.”
Olby and co-senior author Assistant Professor Margaret Gruen, wanted to see if cognitive function could be accurately quantified in dogs.
“Our goal was to bring together multiple tools in order to get a more complete picture of how CCDS presents in dogs,” A/Prof Gruen said.
To accomplish this, they recruited 39 dogs from 15 breeds. All of them were in the senior and geriatric age range, but in good health overall. A dog is considered ‘senior’ if it is in the last 25% of its expected life span based on breed and size, and geriatric beyond that.
The dogs underwent physical and orthopaedic exams, as well as lab work that included a blood test that is a marker of neuronal death. Their owners filled out two commonly used diagnostic questionnaires, and then the dogs participated in a series of cognitive tests designed to assess executive function, memory and attention.
“The approach we took isn’t necessarily designed to be diagnostic; instead, we want to use these tools to be able to identify dogs at an early stage and be able to follow them as the disease progresses, quantifying the changes,” Prof Olby said.
The team found that cognitive and blood test results correlated well with the questionnaire scores, suggesting that a multi-dimensional approach can be used to quantify cognitive decline in aging dogs.
“Being able to diagnose and quantify CCDS in a way that is clinically safe and relevant is a good first step toward being able to work with dogs as a model for Alzheimer’s disease in humans,” Prof Olby said. “Many of the current models of Alzheimers disease – in rodents, for example – are good for understanding physiological changes, but not for testing treatments.”
“Dogs live in our homes and develop naturally occurring disease just like we do,” A/Prof Gruen said. “These findings show promise for both dogs and humans in terms of improving our understanding of disease progression as well as for potentially testing treatments.”