Posts Tagged ‘aging’


Branyas lives in Olot, a city in Catalonia.

By Jack Guy and Al Goodman

A 113-year-old woman, thought to be the oldest in Spain, has said she feels fine after surviving a brush with coronavirus.

Video footage of Maria Branyas, who was born on March 4 1907, shows the super-centenarian speaking to the director of the care home where she lives in Olot, Catalonia.

“In terms of my health I am fine, with the same minor annoyances that anyone can have,” said Branyas in the video. It was recorded Monday, a spokeswoman for the care home told CNN.

Branyas recovered after a mild case of Covid-19. Her battle started shortly after her family visited her on March 4 to celebrate her 113th birthday, the spokeswoman said.

The family has not been able to visit in person since then. Branyas has lived for 18 years in her own private room at the Santa Maria del Tura nursing home, which is run by the Institute of the Order of San Jose of Gerona, affiliated with the Roman Catholic Church, the spokeswoman said.

Branyas was born in San Francisco in the United States, where her father worked as a journalist, reports the AFP news agency.

Over the course of her long life she has survived two world wars as well as the 1918 flu pandemic, which killed more than 50 million people around the world.

Although Branyas recovered from coronavirus, two residents of the same home died of it. The situation at the care home has since improved, said the spokeswoman.

Spain’s state of emergency, in effect since March 14, has strict confinement measures that remain in place. But with the infection and death rates now declining, the government has lifted some lockdown measures in certain parts of the country, on what it says will be a gradual reopening of activity.

But the initial lifting of these restrictions did not apply to Olot, where Branyas lives.

https://www.cnn.com/2020/05/13/europe/spain-oldest-woman-coronavirus-survivor-scli-intl/index.html

By Bukola Adebayo, CNN

A Nigerian woman has given birth to twins, a boy, and a girl at the age of 68.

Margaret Adenuga went through three previous IVF procedures before finally having twins.

Her husband Noah Adenuga, 77 told CNN the couple, who married in 1974 had long desired to have a child of their own.

Adenuga said they never gave up even after the failed attempts.
The retired stock auditor told CNN, “I am a dreamer, and I was convinced this particular dream of ours will come to pass.”

The babies were delivered via caesarian section at 37 weeks last Tuesday at the Lagos University Teaching Hospital (LUTH) but the hospital only recently made the news public to give the first-time mother time to recuperate, it said.

Dr. Adeyemi Okunowo, who delivered the babies, told CNN a specialist team was assembled at the hospital to monitor the pregnancy because of her age.
“As an elderly woman and a first-time mother, it was a high-risk pregnancy and also because she was going to have twins but we were able to manage her pregnancy to term,” Okunowo told CNN.

https://www.cnn.com/2020/04/22/africa/nigerian-woman-68-gives-birth-intl/index.html

Taking up meditation while sheltering-in-place may not only help you cope with the stress of the coronavirus pandemic, it may even keep your brain from aging.

A recently pubished 18-year analysis of the mind of a Buddhist monk by the Center for Healthy Minds at the University of Wisconsin-Madison found daily, intensive meditation slowed the monk’s brain aging by as much as eight years when compared to a control group.

The project started in the 1990s with neuroscientist Richard Davidson’s relationship with the Dalai Lama. Davidson started making connections between positive emotions and brain health, which jump-started research for the study.

“[The Dalai Lama] was really encouraging me to take the practices from this tradition and investigate them with the tools of modern science,” said Davidson, founder and director of the Center for Healthy Minds. “And if we find through these investigations that these practices are valuable to then disseminate them widely.”

The study began with a Buddhist monk

Using MRI and a machine learning framework which estimates “brain-age” from brain imaging, Davidson and lead scientist Nagesh Adluru studied the mind of Tibetan Buddhist meditation master Yongey Mingyur Rinpoche over the course of 18 years.

The goal, Davidson said, was to find out whether there was a difference in the rate of aging between the brains of seasoned meditation masters compared to those who were novice practitioners. Rinpoche was first scanned in 2002 at the age of 27. At the time, he had already completed nine years of meditation retreats. He was scanned again at the respective ages of 30, 32 and 41 years old.

The last time he was scanned, he had just returned from a four-and-a-half-year wandering retreat, and his brain was calculated to be 33-years-old, eight years younger than his biological age.
The researchers compared Rinpoche’s aging brain to a control group and his appeared to age much slower than the general focus group.

The results could have lasting implications on health

The magnitude of the effect was pronounced even with a margin of error that is plus or minus two to three years, Davidson said.

“If these effects accumulate over time, we think there will be very important health and well-being implications.”

Everyone, especially now amid the coronavirus pandemic, can benefit from meditation because it is designed to remind us of our own basic goodness, Davidson said.

“I think what is exciting is the invitation that we can impact our own brain … and change the rate at which it ages through engaging in practices that are nourishing and helpful for our well-being.”

The researchers said they are excited to see how Rinpoche’s brain will continue to develop, and how this data can help improve overall well-being.

https://www.cnn.com/2020/03/20/health/meditation-slows-brain-age-trnd-wellness/index.html

Researchers at the University of Southern California looked at more than 17,000 brain scans to see if daily smoking and drinking advanced brain age. The study found that every gram of alcohol consumed a day aged the brain by 11 days. Smoking a pack of cigarettes a day for a year aged the brain by 11 days. It is one of the largest studies ever done on brain aging and alcohol, making the findings quite robust.

by Shira Feder

Over time, drinking a little bit more alcohol than recommended could accelerate the brain’s aging process, according to a new study.

Though previous studies have found the same, most were tentative findings based on small groups of people or large groups of mice.

The new study, from researchers at the University of Southern California, offers a more robust estimate, reached by examining 17,308 human brain scans from the UK Biobank — one of the biggest sample sizes ever seen.

The team found that for every gram of alcohol consumed a day, the brain aged 0.02 years — or, seven-and-a-half days. (The average can of beer or small glass of wine contains 14 grams of alcohol). People who reported drinking every day had brains which were, on average, 0.4 years older than people who didn’t drink daily.

Smoking had even stronger effect: the team found that those who smoke a pack of cigarettes a day for a year age their brains by 0.03 years (11 days).

The researchers took 30% of the brain scans in their study, all from people aged 45 to 81, and used them to train a computer, which scanned each brain to see how old or young they looked.

They then compared the computer’s estimates of each brain’s age with the person’s real age, and their self-reports of how much alcohol and tobacco they consume daily, in order to see if consuming alcohol or tobacco regularly aged the brain.

Comparing those results with the other 70% of their brain scans, they found that the more you drank and smoke, the more likely you were to have a brain aged beyond your actual age.

Lucina Uddin, director of the Cognitive and Behavioral Neuroscience Division at the University of Miami, who was not involved in the study, told Insider that the use of an algorithm is what makes this study’s findings so compelling.

“Back in the day we’d scan 20 or 40 subjects, if we were lucky, for neuroimaging studies,” Uddin said. “Now we’re getting bigger numbers like 200 or 300 individuals. But this is the biggest sample we’ve ever seen.”

Because the sample size is so big, scientists can ask questions that apply to the entire population, rather than just a few people.

Brain age is essentially a measure of brain health, says Uddin, who was not surprised by the study’s findings.

“Looking at brain age is a way of checking how well you’ve been taking care of your brain,” she told Insider. “My age is 40, but does my brain look more like a 50-year-old brain or a 60-year-old brain? Do you look younger than your age or older than your age?”

The lead author of the study, Arthur Toga, told Inverse: “The 0.4 years of difference was statistically significant. We suggest that daily or almost daily alcohol consumption can be detrimental to the brain.”

However, many super-agers — people who live well beyond 100 years old, and often appear resistant to the dementia gene — report drinking alcohol now and then.

What’s more, a recent Harvard study found drinking in moderation can have some benefits, particularly for the heart.

Dr. Qi Sun, a co-author of the Harvard study, previously told Insider: “If you drink alcohol, it’s very important that you drink responsibly, not in excess, and that you also focus on eating a healthy diet, maintaining a healthy body weight, not smoking, and exercising. If you don’t drink you don’t need to start drinking.”

https://www.insider.com/alcohol-every-day-ages-your-brain-quicker-17000-brain-scans-2020-1

There are no instant, miracle cures. But recent studies suggest we have more control over our cognitive health than we might think. It just takes some effort.

When it comes to battling dementia, the unfortunate news is this: Medications have proven ineffective at curing or stopping the disease and its most common form, Alzheimer’s disease. But that isn’t the end of the story. According to a recent wave of scientific studies, we have more control over our cognitive health than is commonly known. We just have to take certain steps—ideally, early and often—to live a healthier lifestyle.

In fact, according to a recent report commissioned by the Lancet, a medical journal, around 35% of dementia cases might be prevented if people do things including exercising and engaging in cognitively stimulating activities. “When people ask me how to prevent dementia, they often want a simple answer, such as vitamins, dietary supplements or the latest hyped idea,” says Eric Larson, a physician at Kaiser Permanente in Seattle and one of a group of scientists who helped prepare the report. “I tell them they can take many common-sense actions that promote health throughout life.”

The Lancet report, distilling the findings of hundreds of studies, identifies several factors that likely contribute to dementia risk, many of which can be within people’s power to control. These include midlife obesity, physical inactivity, high blood pressure, Type 2 diabetes, social isolation and low education levels.

Of course, there are no guarantees. Dementia is a complicated disease that has multiple causes and risk factors, some of which remain unknown. Nevertheless, there is increasing evidence that people—even those who inherit genes that put them at greater risk of developing Alzheimer’s in later life—can improve their chances by adopting lifestyle changes.

“It’s not just about running three times a week,” says Sarah Lenz Lock, executive director of AARP’s Global Council on Brain Health. “Instead, it’s about a package of behaviors, including aerobic exercise, strength training, a healthy diet, sleep and cognitive training.”

Because most neurodegenerative diseases take years, if not decades, to develop, researchers say the best time to focus on brain health is long before symptoms occur—ideally by midlife if not before. Still, they emphasize that it is never too late to start.

What follows is a look at what scientific studies tell us about possible ways to reduce dementia risk.

1. Blood-pressure control

The potential role that cardiovascular health—including blood pressure—plays in dementia has been one of the tantalizing highlights of recent research based on the Framingham Heart Study, which has followed thousands of residents of Framingham, Mass., and their relatives since 1948.

The research found a 44% decline in the dementia rate among people age 60 or older for the period 2004 to 2008, compared with 1977 to 1983. Diagnoses fell to two for every 100 study participants from 3.6 in the earlier period. Over the same roughly 30 years, the average age at which dementia was diagnosed rose to 85 from 80.

Co-author Claudia Satizabal, an assistant professor at UT Health San Antonio, says the research suggests that improvements in cardiovascular health and education levels help explain the trend. Improvements in dementia rates have occurred only in participants “who had at least a high-school diploma,” the study says. And as dementia rates have fallen, the study also says, so have the rates of “stroke and other cardiovascular diseases,” thanks in part to a greater use of blood-pressure medication.

Unlike studies in which participants are randomly assigned to different treatment groups and then monitored for results, the Framingham study and others that analyze population data cannot definitively prove a cause-and-effect relationship. Dr. Satizabal says that while the significant decline in dementia rates since 1977 suggests that management of stroke and heart issues could have contributed, that “is something that needs more research.”

A recent study that randomly assigned participants to different treatment goals offers further evidence for the idea that high blood pressure is a treatable risk factor that leads to dementia.

In 2010, researchers at Wake Forest School of Medicine began enrolling almost 9,400 people age 50 and older with high blood pressure in one of two groups. With the aid of medication, one group reduced its systolic blood pressure—which measures pressure in the arteries when the heart contracts—to less than 120. The other group aimed for less than 140.

The group with lower blood pressures experienced such significantly lower rates of death, strokes and heart attacks that in 2015 the researchers stopped the trial ahead of schedule. The scientists concluded it would be unethical to continue because most people should be targeting the lower blood pressure, says the study’s co-author Jeff Williamson, a Wake Forest medical school professor.

In 2017 and 2018, the researchers performed a final round of cognitive tests on participants and discovered that the lower-blood-pressure group had 19% fewer diagnoses of mild cognitive impairment, often a precursor to dementia, and 15% fewer cases of any type of dementia, mild or otherwise.

Using MRIs, the researchers scanned 673 participants’ brains and, upon follow-up, found less damaging changes in the lower-blood-pressure group.

“This is the first trial that has demonstrated an effective strategy for prevention of cognitive impairment,” says Kristine Yaffe, professor of psychiatry, neurology and epidemiology at the University of California, San Francisco. “That’s pretty big news,” says Dr. Yaffe, who wasn’t involved in the study.

2. Exercise

Several studies that have followed large numbers of people for years suggest that physically active individuals are less likely than inactive peers are to develop dementia, according to a recent World Health Organization report.

Exercise increases the flow of blood to the brain, improves the health of blood vessels and raises the level of HDL cholesterol, which together help protect against cardiovascular disease and dementia, says Laura Baker, a professor at Wake Forest School of Medicine. Exercise can also lead to the formation of new brain synapses and protect brain cells from dying.

Prof. Baker’s studies suggest that aerobic exercise can help improve cognitive function in people with mild memory, organizational and attention deficits, which are often the first symptoms of cognitive impairment.

One recent study conducted by Prof. Baker and several co-authors enrolled 65 sedentary adults ages 55 to 89 with mild memory problems. For six months, half completed four 60-minute aerobic-exercise sessions at the gym each week. Under a trainer’s supervision, they exercised mainly on treadmills at 70% to 80% of maximum heart rate. The other half did stretching exercises at 35% of maximum heart rate.

At the beginning and end of the study, researchers collected participants’ blood and spinal fluid and obtained MRI scans of their brains. Over the six months, the aerobic-exercise group had a statistically significant reduction in the level in their spinal fluid of tau protein, which accumulates in the brains of people with Alzheimer’s. They also had increased blood flow to areas of the brain that are important for attention and concentration, and their scores on cognitive tests improved. The stretching group, in contrast, showed no improvement on cognitive tests or tau levels.

3. Cognitive training

Many population studies suggest that education increases cognitive reserve, a term for the brain’s ability to compensate for neurological damage. The Framingham study, for example, found that participants with at least a high-school diploma benefited the most from declining dementia rates, compared with participants with less education.

In another population study, researchers at Columbia University analyzed data from 593 people age 60 or older, 106 of whom developed dementia. People with clerical, unskilled or semiskilled jobs had greater risk of getting the disease than managers and professionals.

In a separate study, some of the same researchers followed 1,772 people age 65 or older, 207 of whom developed dementia. After adjusting the results for age, ethnic group, education and occupation, the authors found that people who engaged in more than six activities a month—including hobbies, reading, visiting friends, walking, volunteering and attending religious services—had a 38% lower rate of developing dementia than people who did fewer activities.

In yet another study, researchers at institutions including Rush University Medical Center’s Rush Institute for Healthy Aging examined the brains of 130 deceased people who had undergone cognitive evaluations when alive. Among individuals in whom similar levels of Alzheimer’s-related brain changes were seen in the postmortem examinations, the researchers found that those who had more education generally had shown higher cognitive function.

Yaakov Stern, a professor at Columbia University College of Physicians and Surgeons who has written about these studies and the impact of education on dementia, recommends maintaining “educational and mentally stimulating activities throughout life.” This fosters growth of new neurons and may slow the rate at which certain regions of the brain shrink with age. It also promotes cognitive reserve, he says.

4. Diet

Efforts to study the impact of diet on dementia are relatively new, but there are some indications that certain diets may be beneficial in lowering the risk of dementia.

Several population studies, for instance, suggest that people with a Mediterranean diet, which is high in fish, fruits, nuts and vegetables, have lower rates of dementia, according to the World Health Organization.

But a variation on that diet may offer even more protection against the development of Alzheimer’s disease, according to a study released in 2015.

In this study, researchers including Dr. Martha Clare Morris, director of the Rush Institute for Healthy Aging, analyzed data from 923 people ages 58 to 98 who kept detailed food diaries about what they ate from 2004 to 2013.

In total, 158 subjects developed dementia. But among individuals who remained cognitively healthy, a high proportion had consumed a diet heavy in leafy green and other vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil and wine (in moderation). Their diets were limited in red meat, butter, cheese, sweets and fried and fast foods.

This diet, which researchers named the Mind diet, shares many elements of a Mediterranean diet. But the Mind diet prescribes more foods—including berries and leafy green vegetables—that are associated with lower rates of neurological diseases.

The researchers scored each of the 923 participants on how closely their detailed eating habits followed three diets: Mind, Mediterranean, and Dash diet, designed to reduce high blood pressure. For each diet, researchers ranked the participants based on their scores, subdividing them by the degree to which they followed each diet—closely, partly or little.

This led to several discoveries: First, there were about 50% fewer Alzheimer’s diagnoses among participants who most closely followed either the Mind diet or the Mediterranean diet, compared with those who followed either diet only a little. For the Dash diet, there was a 39% reduction for those who were most faithful to its rules.

Meanwhile, even those who only partly followed the Mind diet saw a 35% reduction in Alzheimer’s diagnoses, while no reduction was seen for those who only partly followed either the Mediterranean or Dash diet.

In contrast to the Mediterranean and Dash diets, “even modest adherence to the Mind diet may have substantial benefits for prevention of Alzheimer’s disease,” says Kristin Gustashaw, a dietitian at Rush.

5. Sleep

No one knows for sure why we sleep. One theory is that sleep helps us remember important information by performing a critical housekeeping function on brain synapses, including eliminating some connections and strengthening others.

Another theory is that sleep washes “toxic substances out of our brains that shouldn’t be there,” including beta amyloid and tau proteins that are implicated in Alzheimer’s, says Ruth Benca, a professor of medicine at the University of California, Irvine.

In a 2015 study, Prof. Benca and others examined 98 participants without dementia ages 50 to 73. Many were at genetic risk for the disease. Brain scans revealed that those reporting more sleep problems had higher levels of amyloid deposits in areas of the brain typically affected by Alzheimer’s.

“Poor sleep may be a risk factor for Alzheimer’s,” says Prof. Benca, who is conducting a study to see whether treating sleep problems may help prevent dementia.

She says sleep—or a lack of it—may help explain why about two-thirds of Alzheimer’s patients are women. Some researchers theorize that during menopause women can become vulnerable to the disease, in part due to increased prevalence of insomnia.

6. Combination

There is a growing consensus that when it comes to preserving brain health, the more healthy habits you adopt, the better.

According to a forthcoming study of 2,765 older adults by researchers at Rush, nonsmokers who stuck to the Mind diet, got regular exercise, engaged in cognitively stimulating activities and drank alcohol in moderation had 60% fewer cases of dementia over six years than people with just one such habit.

A study published in July found that people at greater genetic risk for Alzheimer’s appear to benefit just as much from eating well, exercising and drinking moderately as those who followed the same habits but weren’t at elevated genetic risk for the disease.

The study, by researchers including Kenneth Langa, associate director of the Institute of Gerontology at the University of Michigan, examined data from 196,383 Britons age 60 and older. Over about a decade, there were 38% fewer dementia diagnoses among individuals who had healthy habits and a gene, APOE4, that puts people at higher risk for Alzheimer’s, than there were among people who had the gene and poor habits. The gene increases the risk for Alzheimer’s by two to 12 times, depending on how many copies a person has.

Among participants with low genetic risk for Alzheimer’s, healthy habits were associated with a 40% reduction in the incidence of the disease. The results suggest a correlation between lifestyle, genetic risk and dementia, the study says.

Many point to a recent clinical trial in Finland of 1,260 adults ages 60 to 77 as proof that a multipronged approach can work.

The researchers, from institutions including the Karolinska Institute in Sweden and the National Institute for Health and Welfare in Helsinki, randomly assigned half of the participants, all deemed at high risk for dementia, to regular sessions with nutritionists, exercise trainers and instructors in computerized brain-training programs. The participants attended social events and were closely monitored for conditions including high blood pressure, excess abdominal weight and high blood sugar.

“They got support from each other to make lifestyle changes,” says co-author Miia Kivipelto, a professor at the Karolinska Institute in Sweden.

The other half received only general health advice.

After two years, both groups showed improvements in cognitive performance. But the overall scores of the intensive-treatment group improved by 25% more than the scores for the other group. The intensive-treatment group scored between 40% and 150% better on tests of executive function, mental speed and complex memory tasks, suggesting that a multifaceted approach can “improve or maintain cognitive functioning in at-risk elderly people,” the study says.

“We are studying whether exercise and lifestyle can be medicine to protect brain health as we get older,” says Prof. Baker, who is overseeing a U.S. study modeled on the Finnish trial.

https://apple.news/AzlC5CLNvQJWJrsP-qrJFIw

Our thinking skills in childhood could offer a glimpse into how our minds might work at the age of 70, according to a study spanning decades.

The research started in 1946, when 502 8-year-olds, who were born in the U.K. in the same week, took tests to measure their thinking and memory skills. The participants took cognitive tests again between the ages of 69 and 71.

The participants also had scans, including a positron emission tomography (PET) scan that detects amyloid-beta plaques in the brain. These sticky collections of protein are linked to Alzheimer’s disease.

The study, published in the journal Neurology, shows those with the highest test scores in childhood were more likely to have high scores later in life. Kids in the top 25 percent had a greater chance of being in that same quartile at 70.

Educational attainment and socioeconomic status also appeared to make a difference. Those who were college-educated scored around 16 percent better in tests than those who left school before they hit 16. Participants who had a white-collar job were able to remember, on average, 12 details from a short story, versus 11 if they had a manual job. Overall, women did better than men when their memory and thinking speed were tested.

Participants who were found to have amyloid-beta plaques in their brains, meanwhile, scored lower on cognitive tests. In one assessment where participants had to find the missing pieces in five geometric shapes, those with the plaque got 23 out of 32 problems correct, versus 25 for those without the plaques.

Dr. Jonathan M. Schott of University College London commented: “Finding these predictors is important because if we can understand what influences an individual’s cognitive performance in later life, we can determine which aspects might be modifiable by education or lifestyle changes like exercise, diet or sleep, which may, in turn, slow the development of cognitive decline.

“Our study found that small differences in thinking and memory associated with amyloid plaques in the brain are detectable in older adults even at an age when those who are destined to develop dementia are still likely to be many years away from having symptoms.”

Earlier this year, Schott and his team published a separate study in the journal The Lancet Neurology that showed having high blood pressure in a person’s mid-30s was linked to higher levels of blood vessel damage in the brain, as well as shrinkage of the organ.

Professor Tara Spires-Jones from the UK Dementia Research Institute at the University of Edinburgh, who did not work on the new study, told Newsweek the findings add to other studies that suggest our genetics, as well as environmental factors, play a role in how we maintain our thinking skills as we age.

“However, this does not mean that all of your brain power during aging is determined during childhood,” she said. “There is good scientific evidence from this study and many others that keeping your brain and body active are likely to reduce your risk of developing Alzheimer’s disease, even as adults.”

Learning, socializing and exercise can all help, she said.

“One way this works is by building new connections between brain cells, called synapses. Synapses are the building blocks of memory, so building up a robust network of synapses, sometimes called ‘brain reserve’ is thought to be the biology behind the finding that more education is associated with a lower risk of dementia and age-related cognitive decline,” explained Spires-Jones.

Spires-Jones suggested amyloid-beta plaques might be linked with lower tests scores in the study because they build up and damage the connections between brain cells, called synapses, impairing brain function.

“Amyloid plaques are also widely thought to initiate a toxic cascade that leads to dementia in Alzheimer’s disease, including the build-up and spread of another pathology called ‘tangles,'” she said.

She said the study was “very strong” but limited because observational studies can’t explain the links that emerge, and the participants were all white so the results might not relate to other populations.

“It will be important in future work to try and understand the biological underpinnings for the associations between childhood intelligence and better cognitive ability during aging,” she said.

https://www.newsweek.com/dementia-aging-study-brains-tests-1468657

By Dennis Thompson

Middle-aged folks who worry about healthy aging would do well to keep an eye on their walking speed.

Turns out that the walking speed of 45-year-olds is a pretty solid marker of how their brains and bodies are aging, a new study suggests.

Slow walkers appear to be aging more rapidly, said senior researcher Terrie Moffitt, a professor of psychology and neuroscience at Duke University. They’ve lost more brain volume in middle-age than folks with a quicker walking pace, and also perform worse on physical and mental tests, she said.

“For those people who were slow walkers for their age group, they already had many of the signs of failing health that are regularly tested in a geriatric clinic,” Moffitt said.

In the study, middle-aged people who walked slower than 3.6-feet per second ranked in the lowest fifth when it comes to walking speed, and those are the individuals already showing signs of rapid aging, said Dr. Stephanie Studenski, a geriatrician with the University of Pittsburgh School of Medicine.

“It takes many body systems to have you walk well,” Studenski said. “It takes a good heart, good lungs, good nervous system, good strength, good musculoskeletal system and a variety of other things. Gait speed summarizes the health of all of your body’s systems.”

Gait speed tests are a standard part of geriatric care, and are regularly given to people 65 and older, Moffitt said.

“The slower a person walks, that is a good predictor of impending mortality,” Moffitt said. “The slower they walk, the more likely they will pass away.”

Moffitt and her colleagues suspected that gait tests might be valuable given at an earlier age, figuring that walking speed could serve as an early indicator of how well middle-aged people are aging.

To test this notion, the researchers turned to a long-term study of nearly 1,000 people born in a single year in Dunedin, New Zealand. These people have been tested regularly since their birth in 1972-1973 regarding a wide variety of medical concerns.

This group of study participants recently turned 45, and as they did, the research team tested their walking speed by asking each to repeatedly amble down a 25-foot-long electronic pad, Moffitt said.

Each person walked down the pad at their normal rate, and then again as fast as they could. They also were asked to walk as fast as possible while reciting the alphabet backward, Moffitt said.

All of the participants then were subjected to a battery of aging tests normally used in geriatric clinics.

In addition, they underwent an MRI brain scan to test the volume of their brains, since a shrinking brain has been linked to dementia and Alzheimer’s disease.

The participants also were given a variety of mental and physical tests. The physical tests involved things like balancing on one foot, standing up out of a chair as fast as they could, or gripping a monitor as tightly as they could to test hand strength.

“All these things are very subtle,” Moffitt said. “They’re not anything that would knock you over with a feather. You have to test them in order to find them.”

The findings showed that people who were in the lowest fifth for walking speed had signs of premature and rapid aging.

Studenski said, “It’s the bottom 20% that’s by far in bigger trouble than the others.”

The slower walkers also looked older to a panel of eight screeners asked to guess each participant’s age from a facial photograph.

The findings were published online Oct. 11 in JAMA Network Open.

A gait test could be an easy and low-cost way for primary care doctors to test how well middle-aged patients are aging, said Studenski, who wrote an editorial accompanying the new study.

Doctors could place sensors at the beginning and end of a hallway, and test patients’ walking speed as they head down to the examination room, she added.

However, doctors would need to be taught how to interpret gait speed for middle-aged patients, the same way that geriatricians already are trained to interpret walking speed in seniors.

Middle-aged people with a slower gait could try to slow their aging by eating healthy, exercising, quitting smoking, and maintaining better control over risk factors like high blood pressure and elevated cholesterol, Studenski and Moffitt suggested.

An even better use of walking speed could be as an early test of drugs and therapies meant to counter dementia and other diseases of aging, Moffitt said.

These therapies usually are difficult to assess because researchers have to wait years for people to grow old and display the hoped-for benefits, she noted.

“They need something cheap and effective they can do now to evaluate these treatments,” Moffitt said. “If they give it to people and it speeds up their walking, we’ve really got something there.”

SOURCES: Terrie Moffitt, Ph.D., professor, psychology and neuroscience, Duke University, Durham, N.C.; Stephanie Studenski, M.D., MPH, geriatrician, University of Pittsburgh School of Medicine; Oct. 11, 2019, JAMA Network Open, online

https://consumer.healthday.com/senior-citizen-information-31/misc-aging-news-10/how-fast-you-walk-might-show-how-fast-you-re-aging-751167.html

A study by Stanford University School of Medicine investigators has revealed that immune cells infiltrate the rare newborn nerve-cell nurseries of the aging brain. There’s every reason to think those interlopers are up to no good. Experiments in a dish and in living animals indicate they’re secreting a substance that chokes off new nerve cell production.

While most of the experiments in the study were carried out in mice, the central finding—the invasion, by immune cells called killer T cells, of neurogenic niches (specialized spots in the brain where new nerve cells, or neurons, are generated)—was corroborated in tissue excised from autopsied human brains.

The findings could accelerate progress in hunting down the molecules in the body that promote the common deterioration of brain function in older individuals and in finding treatments that might stall or even reverse that deterioration. They also signify a crack in the wall of dogma that’s deemed the healthy brain impervious to invasion by the body’s immune cells, whose unbridled access to the organ could cause damage.

“The textbooks say that immune cells can’t easily get into the healthy brain, and that’s largely true,” said Anne Brunet, Ph.D., professor of genetics and senior author of the study. “But we’ve shown that not only do they get into otherwise healthy aging brains—including human brains—but they reach the very part of the brain where new neurons arise.”

Lead authorship of the study, to be published online July 3 in Nature, is shared by medical student Ben Dulken, Ph.D., graduate student Matthew Buckley and postdoctoral scholar Paloma Navarro Negredo, Ph.D.

The cells that aid memory

Many a spot in a young mammal’s brain is bursting with brand new neurons. But for the most part, those neurons have to last a lifetime. Older mammals’ brains retain only a couple of neurogenic niches, consisting of several cell types whose mix is critical for supporting neural stem cells that can both differentiate into neurons and generate more of themselves. New neurons spawned in these niches are considered essential to forming new memories and to learning, as well as to odor discrimination.

In order to learn more about the composition of the neurogenic niche, the Stanford researchers catalogued, one cell at a time, the activation levels of the genes in each of nearly 15,000 cells extracted from the subventricular zone (a neurogenic niche found in mice and human brains) of healthy 3-month-old mice and healthy 28- or 29-month-old mice.

This high-resolution, single-cell analysis allowed the scientists to characterize each cell they looked at and see what activities it was engaged in. Their analysis confirmed the presence of nine familiar cell types known to compose the neurogenic niche. But when Brunet and her colleagues compared their observations in the brains of young mice (equivalent in human years to young adults) with what they saw in the brains of old mice (equivalent to people in their 80s), they identified a couple of cell types in the older mice not typically expected to be there—and barely present in the young mice. In particular, they found immune cells known as killer T cells lurking in the older mice’s subventricular zone.

The healthy brain is by no means devoid of immune cells. In fact, it boasts its own unique version of them, called microglia. But a much greater variety of immune cells abounding in the blood, spleen, gut and elsewhere in the body are ordinarily denied entry to the brain, as the blood vessels pervading the brain have tightly sealed walls. The resulting so-called blood-brain barrier renders a healthy brain safe from the intrusion of potentially harmful immune cells on an inflammatory tear as the result of a systemic illness or injury.

“We did find an extremely sparse population of killer T cells in the subventricular zone of young mice,” said Brunet, who is the Michele and Timothy Barakett Endowed Professor. “But in the older mice, their numbers were expanded by 16-fold.”

That dovetailed with reduced numbers of proliferation-enabled neural stem cells in the older mice’s subventricular zone. Further experiments demonstrated several aspects of the killer T cells’ not-so-mellow interaction with neural stem cells. For one thing, tests in laboratory dishware and in living animals indicated that killer T cells isolated from old mice’s subventricular zone were far more disposed than those from the same mice’s blood to pump out an inflammation-promoting substance that stopped neural stem cells from generating new nerve cells.

Second, killer T cells were seen nestled next to neural stem cells in old mice’s subventricular zones and in tissue taken from the corresponding neurogenic niche in autopsied brains of old humans; where this was the case, the neural stem cells were less geared up to proliferate.

Possible brain-based antigens

A third finding was especially intriguing. Killer T cells’ job is to roam through the body probing the surfaces of cells for biochemical signs of a pathogen’s presence or of the possibility that a cell is becoming, or already is, cancerous. Such telltale biochemical features are called antigens. The tens of billions of killer T cells in a human body are able to recognize a gigantic range of antigens by means of receptors on their own surfaces. That’s because every unexposed, or naïve, killer T cell has its own unique receptor shape.

When an initially naïve killer T cell is exposed to an unfamiliar antigen that fits its uniquely shaped receptor, it reacts by undergoing multiple successive rounds of replication, culminating in a large set of warlike cells all sharing the same receptor and all poised to destroy any cells bearing the offending antigen. This process is called clonal expansion.

The killer T cells found in old mice’s brains had undergone clonal expansion, indicating likely exposure to triggering antigens. But the receptors on those killer T cells differed from the ones found in the old mice’s blood, suggesting that the brain-localized killer T cells hadn’t just traipsed through a disrupted blood-brain barrier via passive diffusion but were, rather, reacting to different, possibly brain-based, antigens.

Brunet’s group is now trying to determine what those antigens are. “They may bear some responsibility for the disruption of new neuron production in the aging brain’s neurogenic niches,” she said.

Single cell analysis reveals T cell infiltration in old neurogenic niches, Nature (2019). DOI: 10.1038/s41586-019-1362-5 , https://www.nature.com/articles/s41586-019-1362-5

https://medicalxpress.com/news/2019-07-immune-cells-invade-aging-brains.html


Maria Haverstock, a participant in the Oakland study, became homeless at 58 when she could not find work after leaving an abusive partner.

When Serggio Lanata moved to San Francisco in 2013, he was stunned by its sprawling tent cities. “Homelessness was everywhere I looked,” he says. Lanata, a neurologist at the University of California, San Francisco (UCSF), was also struck by similarities in the behaviour of some older homeless people and patients he had treated for dementia in the clinic. Now, years later, he is embarking on a study that will examine homeless adults for early signs of Alzheimer’s disease and other degenerative brain disorders to better understand the interplay between these conditions and life on the street.

The work, which is set to begin next month, ties into an ongoing effort by researchers at UCSF to understand the biological effects of homelessness in older people. Since 2013, a team led by Margot Kushel, director of the university’s Center for Vulnerable Populations, has followed a group of about 350 older homeless adults in Oakland, California, to determine why this group ages in hyper-speed. Although the participants’ average age is 57, they experience strokes, falls, visual impairment and urinary incontinence at rates typical of US residents in their late 70s and 80s.

The research has drawn attention from politicians, economists and health-care providers across the country who are struggling to help the homeless and reduce their numbers. Although homelessness is a global problem, the situation in California is particularly acute. Nearly 70% of the 130,000 people without homes in the state are considered to be ‘unsheltered’, living on the streets or in locations unfit for human habitation, compared with just 5% in New York City. In the San Francisco Bay Area — California’s wealthy technology hub, which includes Silicon Valley — roughly 28,200 people are homeless.


Homeless encampments, like this one in Oakland, California, are a familiar site in the San Francisco Bay Area.

The United States’ homeless population is also greying: rising housing prices in many areas have increased the rate of homelessness among ‘baby boomers’ born between 1954 and 1964. But many hospitals, police and homeless shelters are unprepared to deal with the special needs of an ageing homeless population. “I hear from shelter providers, ‘Gosh, we are set up for people who use drugs but we have no idea how to manage dementia’,” Kushel says. By understanding how homelessness can accelerate ageing, her team hopes to identify ways to curb suffering and save governments money.

“This crisis is upon us,” says Dennis Culhane, a social scientist at the University of Pennsylvania in Philadelphia. “A lot of money will be spent on this population. We can draw upon Margot’s data and learn how to spend that money wisely — or else we’ll just spend and still have lots of human misery.”

He and his colleagues estimate that Los Angeles, California, will spend $621 million annually on emergency medical care, nursing home beds and shelters for homeless people over the age of 55 between 2019 and 2030. Their analysis suggests that the city could reduce its spending by $33 million per year if it provided homes to elderly people who lack them.

A closer look

Researchers have known for decades that physical and mental health problems are prevalent among the homeless (see ‘Declining health’). But there was little systematic research on the progression and causes of their ailments in 2013, when Kushel launched a study on the life trajectories of older homeless adults in the Bay Area. Since then, 42 of the initial 350 participants have died — mainly from cancer, heart attacks and diabetes. (Earlier this year, the study enrolled another 100 people to compensate for the loss of original participants.)

Kushel and her colleagues got a boost on 1 May, when philanthropists Marc and Lynne Benioff announced that they had donated US$30 million to create a research initiative at UCSF on homelessness. Marc Benioff, who founded the San Francisco-based computing company Salesforce, says the money will support research to explore the causes of homelessness and identify ways to prevent it.

Lanata’s study, which is set to begin next month, will look for signs of debilitating brain conditions — such as dementia of the frontal and temporal lobes, which can cause behavioural changes — in at least 20 homeless adults. He and his colleagues will conduct neurological exams, which might include brain scans, on participants to learn how homelessness influences these brain disorders. People living on the streets might face several factors that can contribute to neurological disease, Lanata says, such as lack of sleep, exposure to polluted air near highways, poorly controlled diabetes, high blood pressure and alcohol abuse.

By asking study participants about their personal histories, he also hopes to learn whether neurological issues might have helped to put them on the street — perhaps by impairing their ability to work or seek government assistance. That would make sense to him, given his experience treating people with some types of dementia. “If those patients didn’t have strong family support, they would be homeless, since no one could or would care for them,” Lanata says. “They can be hard to handle.”

And Kushel has begun a new phase of her ongoing study, which will explore how the sudden stress of homelessness might trigger or exacerbate existing conditions. Many of the people in her study were over the age of 50 when they became homeless.


Kimberly Lea (left) greets Vernada Jones, who is recovering from a gunshot wound to the face. Both women are participating in the Oakland study.

Nearly half of the participants exhibit signs of extreme loneliness, which has been linked to poor outcomes in people with cancer and other diseases1. One-quarter of those in the study meet the criteria for cognitive impairment, compared with less than 10% among people over the age of 70 in the United States more generally2. And in a paper in the press, Kushel and her colleagues found that 10% of participants report being physically or sexually assaulted at least every six months.

An increasing toll

Although Culhane and other health economists have already begun to use Kushel’s findings to project how much it costs to care for the indigent, it is not clear whether politicians or the public will accept such suggestions.

California Governor Gavin Newsom included $500 million for shelters and other support facilities in his proposed $209 billion state budget for 2019–20. But in late March, San Francisco residents rapidly met their goal of raising more than $100,000 to block the construction of a homeless shelter in a wealthy, waterfront neighbourhood. And although city voters approved a plan in November 2018 to fund services for the homeless by taxing the San Francisco’s biggest companies, business groups are challenging the policy in court.

Coco Auerswald, a public-health researcher at the University of California, Berkeley, hopes that Kushel’s work and other studies of homelessness strike a moral nerve. “You judge a society on how it treats its most vulnerable,” she says. “My fear is that we will accept this as a state of affairs in our country.”

Nature 569, 467-468 (2019)

References
1.
Patanwala, M. et al. J. Gen. Intern. Med. 33, 635–643 (2018).

by Lindsey Valich

Explorers have dreamt for centuries of a Fountain of Youth, with healing waters that rejuvenate the old and extend life indefinitely.

Researchers at the University of Rochester, however, have uncovered more evidence that the key to longevity resides instead in a gene.

In a new paper published in the journal Cell, the researchers—including Vera Gorbunova and Andrei Seluanov, professors of biology; Dirk Bohmann, professor of biomedical genetics; and their team of students and postdoctoral researchers—found that the gene sirtuin 6 (SIRT6) is responsible for more efficient DNA repair in species with longer lifespans. The research illuminates new targets for anti-aging interventions and could help prevent age-related diseases.

Inevitable double-strand breaks

As humans and other mammals grow older, their DNA is increasingly prone to breaks, which can lead to gene rearrangements and mutations—hallmarks of cancer and aging. For that reason, researchers have long hypothesized that DNA repair plays an important role in determining an organism’s lifespan. While behaviors like smoking can exacerbate double-strand breaks (DSBs) in DNA, the breaks themselves are unavoidable. “They are always going to be there, even if you’re super healthy,” says Bohmann. “One of the main causes of DSBs is oxidative damage and, since we need oxygen to breathe, the breaks are inevitable.”

Organisms like mice have a smaller chance of accumulating double-strand breaks in their comparatively short lives, versus organisms with longer lifespans, Bohmann says. “But, if you want to live for 50 years or so, there’s more of a need to put a system into place to fix these breaks.”

The longevity gene

SIRT6 is often called the “longevity gene” because of its important role in organizing proteins and recruiting enzymes that repair broken DNA; additionally, mice without the gene age prematurely, while mice with extra copies live longer. The researchers hypothesized that if more efficient DNA repair is required for a longer lifespan, organisms with longer lifespans may have evolved more efficient DNA repair regulators. Is SIRT6 activity therefore enhanced in longer-lived species?

To test this theory, the researchers analyzed DNA repair in 18 rodent species with lifespans ranging from 3 years (mice) to 32 years (naked mole rats and beavers). They found that the rodents with longer lifespans also experience more efficient DNA repair because the products of their SIRT6 genes—the SIRT6 proteins—are more potent. That is, SIRT6 is not the same in every species. Instead, the gene has co-evolved with longevity, becoming more efficient so that species with a stronger SIRT6 live longer. “The SIRT6 protein seems to be the dominant determinant of lifespan,” Bohmann says. “We show that at the cell level, the DNA repair works better, and at the organism level, there is an extended lifespan.”

The researchers then analyzed the molecular differences between the weaker SIRT6 protein found in mice versus the stronger SIRT6 found in beavers. They identified five amino acids responsible for making the stronger SIRT6 protein “more active in repairing DNA and better at enzyme functions,” Gorbunova says. When the researchers inserted beaver and mouse SIRT6 into human cells, the beaver SIRT6 better reduced stress-induced DNA damage compared to when researchers inserted the mouse SIRT6. The beaver SIRT6 also better increased the lifespan of fruit flies versus fruit flies with mouse SIRT6.

Species with even more robust SIRT6?

Although it appears that human SIRT6 is already optimized to function, “we have other species that are even longer lived than humans,” Seluanov says. Next steps in the research involve analyzing whether species that have longer lifespans than humans—like the bowhead whale, which can live more than 200 years—have evolved even more robust SIRT6 genes.

The ultimate goal is to prevent age-related diseases in humans, Gorbunova says. “If diseases happen because of DNA that becomes disorganized with age, we can use research like this to target interventions that can delay cancer and other degenerative diseases.”

https://phys.org/news/2019-04-longevity-gene-responsible-efficient-dna.html