There are many reasons to avoid getting diabetes, or to keep it controlled if you already have it: Higher risks for heart disease, stroke and for having a foot or leg amputation. But here’s another one: It’s a major risk factor for dementia.
While researchers are still investigating what causes that increased risk, one thing they do know is it’s linked to highs – and lows – in the body’s blood sugar levels.
“Whether it’s Type 1 or Type 2 diabetes, glycemic control is very important” for maintaining good brain health, said Rachel Whitmer, chief of the division of epidemiology at University of California, Davis and associate director of the school’s Alzheimer’s Disease Research Center. “This is another motivation to have good control.”
Good management of blood glucose levels is one of seven lifestyle changes people can make to support better heart and brain health, called Life’s Simple 7 by the American Heart Association. It’s a step that could potentially help more than 34.2 million people in the U.S. living with diabetes.
Contrary to what science once suggested, older people with a declining sense of smell do not have comprehensively dampened olfactory ability for odors in general – it simply depends upon the type of odor. Researchers at the University of Copenhagen reached this conclusion after examining a large group of older Danes’ and their intensity perception of common food odors.
That grandpa and grandma aren’t as good at smelling as they once were, is something that many can relate to. And, it has also been scientifically demonstrated. One’s sense of smell gradually begins to decline from about the age of 55. Until now, it was believed that one’s sense of smell broadly declined with increasing age. However, a study from the University of Copenhagen reports that certain food odors are significantly more affected than others.
The Department of Food Science’s Eva Honnens de Lichtenberg Broge and her fellow researchers have tested the ability of older Danes to perceive everyday food odors. The researchers measured how intensely older adults perceived different food odours, as well as how much they liked the odours.
Researchers from Tokyo Metropolitan University have discovered that a specific chemical feature of a key protein known as tau may cause it to accumulate in the brain and trigger illnesses like Alzheimer’s. They found that disulfide bonds on certain amino acids act to stabilize tau and cause it to accumulate, an effect that got worse with increased oxidative stress. The identification of chemical targets triggering tau accumulation may lead to breakthrough treatments.
The tau protein is key to the healthy function of biological cells. It helps form and stabilize microtubules, the thin filaments that crisscross cell interiors to help keep them structurally rigid and provide ‘highways’ to shuttle molecules between organelles. However, when they are not formed correctly, they can accumulate and form sticky clumps. In the brain, these aggregates block the firing of neurons and cause a wide range of neurodegenerative diseases known as tauopathies, one of which is Alzheimer’s disease. It is vastly important that scientists find the ‘switch’ that transforms tau from an indispensable part of cell function to a deadly pathology.
A team led by Associate Professor Kanae Ando of Tokyo Metropolitan University has been using model organisms like the Drosophila fruit fly to uncover how specific features of the tau protein cause it to stop working properly. Flies can be genetically altered to express the same tau protein as in humans. By systematically modifying parts of the gene encoding for tau, they have been trying to pinpoint how certain features of mutant tau proteins affect their behavior.
In their most recent work, they found that alterations to amino acid residues in the protein known as cysteines in two different locations (C291 and C322) had a drastic effect on the amount and toxicity of tau. In a further breakthrough, the team pinned down the specific chemical feature responsible for making them toxic to normal cell function, that is, disulfide bonds formed by these cysteine groups. The toxic accumulation of tau got worse when cells were put in an environment with elevated levels of reactive oxygen species, as thiol groups on the cysteines were oxidized to form disulfide links. Biochemical environments with elevated oxidative stress are similar to those seen in patients with tauopathies. The co-expression of antioxidants to counter this effect helped natural processes clear away tau proteins, resulting in dramatically lower tau levels.
The team hope that knowledge of exactly which chemical groups are responsible for tau toxicity may lead to novel therapies which reduce or prevent tau accumulation, helping sufferers of tauopathies around the world.
Legend has it that Marie Antoinette’s hair turned gray overnight just before her beheading in 1791.
Though the legend is inaccurate–hair that has already grown out of the follicle does not change color–a new study from researchers at Columbia University Vagelos College of Physicians and Surgeons is the first to offer quantitative evidence linking psychological stress to graying hair in people.
And while it may seem intuitive that stress can accelerate graying, the researchers were surprised to discover that hair color can be restored when stress is eliminated, a finding that contrasts with a recent study in mice that suggested that stressed-induced gray hairs are permanent.
The study, published June 22 in eLife, has broader significance than confirming age-old speculation about the effects of stress on hair color, says the study’s senior author Martin Picard, PhD(link is external and opens in a new window), associate professor of behavioral medicine (in psychiatry and neurology) at Columbia University Vagelos College of Physicians and Surgeons.
“Understanding the mechanisms that allow ‘old’ gray hairs to return to their ‘young’ pigmented states could yield new clues about the malleability of human aging in general and how it is influenced by stress,” Picard says.
Sarcopenia, the gradual loss of muscle mass that can occur with aging, affects 15 percent of people over age 65, and 50 percent of people over age 80. As we lose muscle mass, we lose strength, and if we lose too much, our ability to function suffers. Fortunately, emerging research is shedding new light on the role dietary protein plays in maintaining muscle, functionality, and health as we age.
Some of this gradual, age-associated loss of muscle mass, strength, and function has to do with a decrease in activity, but not all of it. “Like many complex syndromes of older adults, many factors contribute to sarcopenia,” says Roger A. Fielding, PhD, director of the Human Nutrition Research Center on Aging (HNRCA) Nutrition, Exercise Physiology and Sarcopenia laboratory. “Decreased physical activity, hormonal changes, increase in low-grade inflammatory processes, and changes in dietary intake that include decline in protein intake are all involved.”
Protein and Muscle: The body’s ability to manufacture muscle from protein decreases a bit with aging, so increasing dietary protein—in concert with muscle-building exercise—could help to maintain muscle mass and strength. “We know that in extreme conditions of protein malnutrition people lose muscle mass pretty rapidly,” says Fielding. “But even in older individuals who are taking in protein around the recommended levels, consuming lower amounts of protein is associated with higher rate of muscle loss than consuming higher amounts of protein.”
Paul F. Jacques, DSc, a professor at the Friedman School of Nutrition Science and Policy and senior scientist at the HNRCA Nutritional Epidemiology Team, and his colleagues found higher protein intake may translate to less frailty, disability, or physical dysfunction “We found that higher protein intake was associated with a 30 percent lower risk of losing functional integrity with time,” says Jacques. “This is observational data, but it clearly demonstrates the potential importance of a higher protein diet.”
A strange thing sometimes happens when we listen to a spoken phrase again and again: It begins to sound like a song.
This phenomenon, called the “speech-to-song illusion,” can offer a window into how the mind operates and give insight into conditions that affect people’s ability to communicate, like aphasia and aging people’s decreased ability to recall words.
Now, researchers from the University of Kansas have published a study in PLOS ONE examining if the speech-to-song illusion happens in adults who are 55 or older as powerfully as it does with younger people.
The KU team recruited 199 participants electronically on Amazon’s Mechanical Turk (MTurk), a website used to conduct research in the field of psychology. The subjects listened to a sound file that exemplified the speech-to-song illusion, then completed surveys relating to three different studies.
“In the first study, we just played them the canonical stimulus made by the researcher that discovered this illusion — if that can’t create the illusion, then nothing can,” said co-author Michael Vitevitch, professor of psychology at KU. “Then we simply asked people, ‘Did you experience the illusion or not?’ There was no difference in the age of the number of people that said yes or no.”
Because I have people onboth sides of my family who have suffered from Alzheimer’s or dementia, I know I am particularly sensitive to my cognitive state. But, I think that is typical of everyone over 50 years old.
Misplacing keys. Forgetting names. Struggling to find the right word. Walking into a room and forgetting why.
Are these early signs of dementia? Or normal signs of aging?
It all depends on the circumstances, health experts say. To distinguish between changes associated with typical aging and concerning signs of cognitive loss requires a deeper look.
“Instead of thinking about things in terms of what is a sign of dementia, I would ask, ‘What is the situation in which those signs appear?'” said Dr. Jeffrey Keller, founder and director of the Institute for Dementia Research and Prevention in Baton Rouge, Louisiana. “It’s how the brain functions in response to a challenge that demonstrates early changes that can lead to dementia.”
In other words, a person experiencing normal aging may experience some memory lapses, he said. But more important than whether they’ve misplaced their keys is whether they’re able to retrace their steps to find them. Or whether they can retain information long enough to carry out a multi-part task, such as filling out medical or tax forms, even if interrupted while doing so.
People who feel younger have a greater sense of well-being, better cognitive functioning, less inflammation, lower risk of hospitalization and even live longer than their older-feeling peers. A study published by the American Psychological Association suggests one potential reason for the link between subjective age and health: Feeling younger could help buffer middle-aged and older adults against the damaging effects of stress.
In the study, published in Psychology and Aging, researchers from the German Centre of Gerontology analyzed three years of data from 5,039 participants in the German Ageing Survey, a longitudinal survey of residents of Germany age 40 and older. The survey included questions about the amount of perceived stress in peoples’ lives and their functional health – how much they were limited in daily activities such as walking, dressing and bathing. Participants also indicated their subjective age by answering the question, “How old do you feel?”
The researchers found, on average, participants who reported more stress in their lives experienced a steeper decline in functional health over three years, and that link between stress and functional health decline was stronger for chronologically older participants.
However, subjective age seemed to provide a protective buffer. Among people who felt younger than their chronological age, the link between stress and declines in functional health was weaker. That protective effect was strongest among the oldest participants.
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.