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.
A natural compound previously demonstrated to counteract aspects of aging and improve metabolic health in mice has clinically relevant effects in people, according to new research at Washington University School of Medicine in St. Louis.
A small clinical trial of postmenopausal women with prediabetes shows that the compound NMN (nicotinamide mononucleotide) improved the ability of insulin to increase glucose uptake in skeletal muscle, which often is abnormal in people with obesity, prediabetes or Type 2 diabetes. NMN also improved expression of genes that are involved in muscle structure and remodeling. However, the treatment did not lower blood glucose or blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, reduce fat in the liver or decrease circulating markers of inflammation as seen in mice.
The study, published online April 22 in the journal Science, is the first randomized clinical trial to look at the metabolic effects of NMN administration in people.
Among the women in the study, 13 received 250 mg of NMN orally every day for 10 weeks, and 12 were given an inactive placebo every day over the same period.
Aging entails a loss of muscle mass and strength, which in some cases impairs mobility, hinders walking or performance of day-to-day tasks, and exposes the elderly to the risk of falls and hospitalizations.
In clinical practice, handgrip measurement is the most widely used method to identify loss of overall muscular strength in older people. Values below 26 kg for men and 16 kg for women have for some time been considered an indication of risk-associated weakness, but these parameters are being revised.
Researchers at the Federal University of São Carlos (UFSCar) in the state of São Paulo, Brazil, collaborating with colleagues at other institutions in the same state such as the University of São Paulo’s Ribeirão Preto Medical School (FMRP-USP), Nursing School (EE-USP) and School of Public Health (FSP-USP), as well as University College London (UCL), have suggested higher handgrip cutoff values than those typically used by physicians, physical therapists and nutritionists. A higher cutoff permits early diagnosis and intervention to avert clinical progression.
Getting a flu vaccine can reduce the risk of a common type of heart attack in people 60 and older, according to new research that suggests the virus plays a role in rupturing plaque.
In a study published Thursday in the Journal of the American Heart Association, researchers in Spain used data from five consecutive flu seasons and zeroed in on 8,240 people who had Type 1 heart attacks. They found flu and cold temperatures were each independently associated with an increased risk of that kind of heart attack, and flu shots could reduce that risk among people 60 and up.
“Our results suggest influenza viruses play a major role in plaque rupture,” said study author Dr. J Alberto García-Lledó, head of cardiology at Hospital Universitario Príncipe de Asturias in Madrid. “The study reinforces the need to conduct prevention campaigns during cold waves and influenza seasons. The most important prevention tool we have is influenza vaccination.”
Neurons lack the ability to replicate their DNA, so they’re constantly working to repair damage to their genome. Now, a new study by Salk scientists finds that these repairs are not random, but instead focus on protecting certain genetic “hot spots” that appear to play a critical role in neural identity and function, according to Science Daily.
The findings, published in the April 2, 2021, issue of Science, give novel insights into the genetic structures involved in aging and neuro-degeneration, and could point to the development of potential new therapies for diseases such Alzheimer’s, Parkinson’s and other age-related dementia disorders.
“This research shows for the first time that there are sections of genome that neurons prioritize when it comes to repair,” says Professor and Salk President Rusty Gage, the paper’s co-corresponding author. “We’re excited about the potential of these findings to change the way we view many age-related diseases of the nervous system and potentially explore DNA repair as a therapeutic approach.”
It ought to be a no-brainer, so to speak: Research has pinpointed seven ways people can achieve ideal heart and brain health. And – bonus – if Americans did those things, they also could help prevent many other chronic illnesses, According to the American Heart Association News.
But most people don’t, at least not consistently. What’s stopping them?
“Most of these steps require a great deal of self-regulation and self-control,” said Dolores Albarracin, a professor of psychology at the University of Illinois at Urbana-Champaign. “It’s not just getting one thing done, like going to get a vaccine, where you can do it and forget about it for a year.”
Volumes of research point to at least seven behaviors, called Life’s Simple 7, that can dramatically lower the burden of heart disease, stroke and dementia. Not smoking, eating a healthy diet, exercising regularly, maintaining a healthy weight, and keeping blood glucose, blood pressure and cholesterol levels in a healthy range have the potential to collectively wipe out a vast majority of heart disease and stroke and prevent or delay a significant number of dementias.
Primary care doctors can play an important role in helping to preserve brain health by encouraging healthy behaviors and addressing risk factors associated with cognitive decline, according to a new scientific report.
The American Heart Association statement published in the journal Stroke outlines seven lifestyle targets and six risk factors for brain health that primary care doctors should address in adults of all ages. The statement also has been endorsed by the American Academy of Neurology as an educational tool for neurologists.
As the nation ages, preserving brain health has become a growing concern. Mild cognitive impairment affects an estimated 1 in 5 Americans age 65 and older; 1 in 7 has dementia – a number expected to triple by 2050.
“Primary care is the right home for practice-based efforts to prevent or postpone cognitive decline,” Ronald Lazar, chair of the scientific statement writing group, said in a news release. Lazar directs the Evelyn F. McKnight Brain Institute at the University of Alabama at Birmingham.
“Prevention doesn’t start in older age; it exists along the health care continuum from pediatrics to adulthood,” he said. “The evidence in this statement demonstrates that early attention to these factors improves later life outcomes.”
The statement asks primary care doctors to integrate brain health into their treatment of adults guided by the AHA’s Life’s Simple 7, a collection of lifestyle targets shown to help achieve ideal heart and brain health. These include managing blood pressure, cholesterol and blood sugar levels; increasing physical activity; eating a healthy diet; losing weight; and not smoking.
The statement also asks them to assess their patients’ risk factors for cognitive health, including depression, social isolation, excessive alcohol use, sleep disorders, lower education levels and hearing loss.
“Scientists are learning more about how to prevent cognitive decline before changes to the brain have begun,” Lazar, a professor of neurology and neurobiology, said. “We have compiled the latest research and found Life’s Simple 7 plus other factors like sleep, mental health and education are a more comprehensive lifestyle strategy that optimizes brain health in addition to cardiovascular health.”
Dr. Deborah Levine, one of the statement’s co-authors, said it is never too soon to target risk factors for ideal heart and brain health. It’s also never too late.
“For example, lower blood pressure levels reduce the risk of cognitive impairment and dementia in older adults,” she said. “In adults of all ages, the metrics in Life’s Simple 7 prevent stroke, and stroke increases the risk of dementia by more than twofold.”
Additional risk factors can help physicians identify which patients may need special attention, said Levine, an associate professor of medicine at the University of Michigan Medical School in Ann Arbor.
For example, “Primary care doctors can help their patients reduce dementia risk by identifying and aggressively treating vascular risk factors like high blood pressure. Black and Hispanic individuals, women and individuals with lower educational levels appear at higher risk for dementia, so these high-risk groups are a top priority,” Levine said.
According to the statement, recent research shows high blood pressure, diabetes and smoking in adulthood and midlife increase the odds of cognitive decline in middle age. And they accelerate cognitive decline in older age.
“Many people think of high blood pressure, Type 2 diabetes and other risk factors as affecting only heart health, yet these very same risk factors affect our brain health,” Lazar said. “Patients might be more likely to pay attention to the importance of addressing modifiable risk factors if they understood the links.”
The statement defines brain health using the term cognition, which includes memory, thinking, reasoning, communication and problem-solving.
Together, these functions enable people to navigate the everyday world, according to the report. The ability to think, solve problems, remember, perceive and communicate are crucial to successful living; their loss can lead to helplessness and dependency.
“Studies have shown that these domains are impacted by factors that are within our control to change,” Lazar said. “Prevention and mitigation are important, because once people have impaired cognition, the current treatment options are very limited.”
If you believe you are capable of becoming the healthy, engaged person you want to be in old age, you are much more likely to experience that outcome, a recent Oregon State University study shows.
“How we think about who we’re going to be in old age is very predictive of exactly how we will be,” said Shelbie Turner, a doctoral student in OSU’s College of Public Health and Human Sciences and co-author on the study.
Previous studies on aging have found that how people thought about themselves at age 50 predicted a wide range of future health outcomes up to 40 years later — cardiovascular events, memory, balance, will to live, hospitalizations; even mortality.
“Previous research has shown that people who have positive views of aging at 50 live 7.5 years longer, on average, than people who don’t,” said Karen Hooker, co-author of the study and the Jo Anne Leonard Petersen Endowed Chair in Gerontology and Family Studies at OSU.
Because self-perceptions of aging are linked to so many major health outcomes, Hooker and Turner wanted to understand what influences those perceptions. Their study looked specifically at the influence of two factors: self-efficacy associated with possible selves, meaning a person’s perceived ability to become the person they want to be in the future; and optimism as a general personality trait.
A new model of aging takes into account not only genetics and environmental exposures but also the tiny changes that randomly arise at the cellular level.
University Professor Caleb Finch introduced the “Tripartite Phenotype of Aging” as a new conceptual model that addresses why lifespan varies so much, even among human identical twins who share the same genes. Only about 10 to 35 percent of longevity can be traced to genes inherited from our parents, Finch mentioned.
Finch authored the paper introducing the model with one of his former graduate students, Amin Haghani, who received his PhD in the Biology of Aging from the USC Leonard Davis School in 2020 and is now a postdoctoral researcher at UCLA. In the article, they propose that the limited heritability of aging patterns and longevity in humans is an outcome of gene-environment interactions, together with stochastic, or chance, variations in the body’s cells. These random changes can include cellular changes that happen during development, molecular damage that occurs later in life, and more.
Patients suffering from dry eye disease symptoms have a lower quality of life compared to those without symptoms, a new study reports. The findings showed that patients with the condition reported negative effects on visual function, their ability to carry out daily activities and their work productivity.
Dry eye disease is a common condition and a frequent reason for patients to seek medical care. It can affect people of any age but is most prevalent in women and in older people. Symptoms include irritation and redness in the eyes, blurred vision, and a sensation of grittiness or a foreign body in the eye. It has been reported that up to a third of adults over 65 years old have the condition, although the actual number is likely to be higher as there is no established diagnostic test and people with mild symptoms are less likely to report them to their doctor.
Treatment often involves prescriptions of artificial tears, ocular lubricants and astringents, which come at a cost to the NHS; in 2014, 6.4 million items were prescribed at a cost of over £27 million.
This new study, led by the University of Southampton, set out to explore how dry eye disease affects the lives of adults in the UK through an online survey of one thousand patients with the condition and further one thousand without. Participants undertook a questionnaire from the National Eye Institute about their visual function and a EuroQol questionnaire on health-related quality of life. Those who declared that they experienced dry eye disease also answered further questions to assess the severity of their symptoms.
A new study led by the University of Portsmouth has identified that one of the major factors of age-related brain deterioration is the loss of a substance called myelin.
Myelin acts like the protective and insulating plastic casing around the electrical wires of the brain – called axons. Myelin is essential for superfast communication between nerve cells that lie behind the supercomputer power of the human brain.
The loss of myelin results in cognitive decline and is central to several neurodegenerative diseases, such as Multiple Sclerosis and Alzheimer’s disease. This new study found that the cells that drive myelin repair become less efficient as we age and identified a key gene that is most affected by ageing, which reduces the cells ability to replace lost myelin.
The gut microbiome is an integral component of the body, but its importance in the human aging process is unclear. Institute for Systems Biology (ISB) researchers and their collaborators have identified distinct signatures in the gut microbiome that are associated with either healthy or unhealthy aging trajectories, which in turn predict survival in a population of older individuals. The work was just published in the journal Nature Metabolism,
The research team analyzed gut microbiome, phenotypic and clinical data from over 9,000 people – between the ages of 18 and 101 years old – across three independent cohorts. The team focused, in particular, on longitudinal data from a cohort of over 900 community-dwelling older individuals (78-98 years old), allowing them to track health and survival outcomes.
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.
A new large scale genetic analysis has found biological mechanisms that contribute to making people more susceptible to muscle weakness in later life, finding that diseases such as osteoarthritis and diabetes may play a large role in susceptibility.
As we get older we lose muscle strength, and in some people this severe weakness impacts their ability to live everyday lives, a condition called sarcopenia. Around 10 per cent of people over 50 experience sarcopenia. Many causes thought to impact likelihood of developing this weakness, which is linked to higher death rates.
In a genetic analysis of over 250,000 people aged over 60 from UK Biobank and 21 other cohorts, an international team led by researchers at the University of Exeter looked at hand grip strength, using thresholds of loss of muscle function derived from international definitions of sarcopenia.
The team, including collaborators from the USA and the Netherlands, then conducted a genetic analysis, and found specific biological mechanisms push some people towards sarcopenia, while protecting others. The study, published in Nature Communications identified 15 areas of the genome, or loci, associated with muscle weakness, including 12 loci not implicated in previous analyses of continuous measures of grip strength.
Biomarkers in the blood including red blood cells and inflammation may also share causal pathways with sarcopenia. Together, these results highlight specific areas for intervention or for identifying those at most risk.
Lead author Garan Jones said: “The strongest associations we found were close to regions of the genome regulating the immune system, and growth and development of the muscloskeletal system. However, we also discovered associations with regions not previously known to be linked to muscloskeletal traits.
“We found that our analysis of muscle weakness in older people shared common genetic pathways with metabolic diseases such as type-2 diabetes, and auto-immune conditions such as osteoarthritis and rheumatoid arthritis. In subgroups of people with increased risk of these conditions, sarcopenia may be a key outcome to look out for and prevent.
“We hope that by understanding the genetic contributions to muscle weakness with age, we will be able to highlight possible therapeutic interventions earlier in life, which would lead to a happier and healthier old age.”
Evidence is mounting to suggest that some helminth worms are ‘old friend’ commensals that can help us fight inflammation and prevent age-related disease.
Parasitic worms could hold the key to living longer and free of chronic disease, according to a review article published in the open-access eLife journal.
The review looks at the growing evidence to suggest that losing our ‘old friend’ helminth parasites, which used to live relatively harmlessly in our bodies, can cause ageing-associated inflammation. It raises the possibility that carefully controlled, restorative helminth treatments could prevent ageing and protect against diseases such as heart disease and dementia.
“A decline in exposure to commensal microbes and gut helminths in developed countries has been linked to increased prevalence of allergic and autoimmune inflammatory disorders – the so-called ‘old friends hypothesis’,” explains author Bruce Zhang, Undergraduate Assistant at the UCL Institute of Healthy Ageing, London, UK. “A further possibility is that this loss of ‘old friend’ microbes and helminths increases the sterile, ageing-associated inflammation known as inflammageing.”
Many people worry about not being able to move around as well when they get older. They fear they won’t be able to continue their favorite activities, visit their favorite places, or even keep up with everyday tasks.
Mobility — the ability to move or walk freely and easily — is critical for functioning well and living independently. As we age, we may experience changes to our mobility. There are many reasons for these changes, including changes in gait (how we walk), balance, and physical strength.
All of these can increase the number and severity of falls and make it harder for older adults to go out and visit with friends and family and continue doing their activities independently. Older adults who lose their mobility are less likely to remain living at home; have higher rates of disease, disability, hospitalization, and death; and have poorer quality of life.
Researchers are working on this issue because it’s not only a matter of physical health, but also the social and emotional well-being of older adults.
NIA-supported researchers are identifying risk factors for physical disability and developing and testing ways to prevent or reverse loss of mobility to help older adults maintain independence. For example, long-running observational studies, such as the Women’s Health and Aging Study II and the Health, Aging, and Body Composition Study, examine functional decline and how it differs by race and sex.