Posts Tagged ‘aging’

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

Advertisements

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

By Emily Underwood

One of the thorniest debates in neuroscience is whether people can make new neurons after their brains stop developing in adolescence—a process known as neurogenesis. Now, a new study finds that even people long past middle age can make fresh brain cells, and that past studies that failed to spot these newcomers may have used flawed methods.

The work “provides clear, definitive evidence that neurogenesis persists throughout life,” says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto, Canada. “For me, this puts the issue to bed.”

Researchers have long hoped that neurogenesis could help treat brain disorders like depression and Alzheimer’s disease. But last year, a study in Nature reported that the process peters out by adolescence, contradicting previous work that had found newborn neurons in older people using a variety of methods. The finding was deflating for neuroscientists like Frankland, who studies adult neurogenesis in the rodent hippocampus, a brain region involved in learning and memory. It “raised questions about the relevance of our work,” he says.

But there may have been problems with some of this earlier research. Last year’s Nature study, for example, looked for new neurons in 59 samples of human brain tissue, some of which came from brain banks where samples are often immersed in the fixative paraformaldehyde for months or even years. Over time, paraformaldehyde forms bonds between the components that make up neurons, turning the cells into a gel, says neuroscientist María Llorens-Martín of the Severo Ochoa Molecular Biology Center in Madrid. This makes it difficult for fluorescent antibodies to bind to the doublecortin (DCX) protein, which many scientists consider the “gold standard” marker of immature neurons, she says.

The number of cells that test positive for DCX in brain tissue declines sharply after just 48 hours in a paraformaldehyde bath, Llorens-Martín and her colleagues report today in Nature Medicine. After 6 months, detecting new neurons “is almost impossible,” she says.

When the researchers used a shorter fixation time—24 hours—to preserve donated brain tissue from 13 deceased adults, ranging in age from 43 to 87, they found tens of thousands of DCX-positive cells in the dentate gyrus, a curled sliver of tissue within the hippocampus that encodes memories of events. Under a microscope, the neurons had hallmarks of youth, Llorens-Martín says: smooth and plump, with simple, undeveloped branches.

In the sample from the youngest donor, who died at 43, the team found roughly 42,000 immature neurons per square millimeter of brain tissue. From the youngest to oldest donors, the number of apparent new neurons decreased by 30%—a trend that fits with previous studies in humans showing that adult neurogenesis declines with age. The team also showed that people with Alzheimer’s disease had 30% fewer immature neurons than healthy donors of the same age, and the more advanced the dementia, the fewer such cells.

Some scientists remain skeptical, including the authors of last year’s Nature paper. “While this study contains valuable data, we did not find the evidence for ongoing production of new neurons in the adult human hippocampus convincing,” says Shawn Sorrells, a neuroscientist at the University of Pittsburgh in Pennsylvania who co-authored the 2018 paper. One critique hinges on the DCX stain, which Sorrells says isn’t an adequate measure of young neurons because the DCX protein is also expressed in mature cells. That suggests the “new” neurons the team found were actually present since childhood, he says. The new study also found no evidence of pools of stem cells that could supply fresh neurons, he notes. What’s more, Sorrells says two of the brain samples he and his colleagues looked at were only fixed for 5 hours, yet they still couldn’t find evidence of young neurons in the hippocampus.

Llorens-Martín says her team used multiple other proteins associated with neuronal development to confirm that the DCX-positive cells were actually young, and were “very strict,” in their criteria for identifying young neurons.

Heather Cameron, a neuroscientist at the National Institute of Mental Health in Bethesda, Maryland, remains persuaded by the new work. Based on the “beauty of the data” in the new study, “I think we can all move forward pretty confidently in the knowledge that what we see in animals will be applicable in humans, she says. “Will this settle the debate? I’m not sure. Should it? Yes.”

https://www.sciencemag.org/news/2019/03/new-neurons-life-old-people-can-still-make-fresh-brain-cells-study-finds?utm_campaign=news_daily_2019-03-25&et_rid=17036503&et_cid=2734364

A team from the Department of Psychological Medicine and Department of Biochemistry at the Yong Loo Lin School of Medicine at the National University of Singapore (NUS) has found that seniors who consume more than two standard portions of mushrooms weekly may have 50 per cent reduced odds of having mild cognitive impairment (MCI).

A portion was defined as three quarters of a cup of cooked mushrooms with an average weight of around 150 grams. Two portions would be equivalent to approximately half a plate. While the portion sizes act as a guideline, it was shown that even one small portion of mushrooms a week may still be beneficial to reduce chances of MCI.

“This correlation is surprising and encouraging. It seems that a commonly available single ingredient could have a dramatic effect on cognitive decline,” said Assistant Professor Lei Feng, who is from the NUS Department of Psychological Medicine, and the lead author of this work.

The six-year study, which was conducted from 2011 to 2017, collected data from more than 600 Chinese seniors over the age of 60 living in Singapore. The research was carried out with support from the Life Sciences Institute and the Mind Science Centre at NUS, as well as the Singapore Ministry of Health’s National Medical Research Council. The results were published online in the Journal of Alzheimer’s Disease on 12 March 2019.

Determining MCI in seniors

MCI is typically viewed as the stage between the cognitive decline of normal ageing and the more serious decline of dementia. Seniors afflicted with MCI often display some form of memory loss or forgetfulness and may also show deficit on other cognitive function such as language, attention and visuospatial abilities. However, the changes can be subtle, as they do not experience disabling cognitive deficits that affect everyday life activities, which is characteristic of Alzheimer’s and other forms of dementia.

“People with MCI are still able to carry out their normal daily activities. So, what we had to determine in this study is whether these seniors had poorer performance on standard neuropsychologist tests than other people of the same age and education background,” explained Asst Prof Feng. “Neuropsychological tests are specifically designed tasks that can measure various aspects of a person’s cognitive abilities. In fact, some of the tests we used in this study are adopted from commonly used IQ test battery, the Wechsler Adult Intelligence Scale (WAIS).”

As such, the researchers conducted extensive interviews and tests with the senior citizens to determine an accurate diagnosis. “The interview takes into account demographic information, medical history, psychological factors, and dietary habits. A nurse will measure blood pressure, weight, height, handgrip, and walking speed. They will also do a simple screen test on cognition, depression, anxiety,” said Asst Prof Feng.

After this, a two-hour standard neuropsychological assessment was performed, along with a dementia rating. The overall results of these tests were discussed in depth with expert psychiatrists involved in the study to get a diagnostic consensus.

Mushrooms and cognitive impairment

Six commonly consumed mushrooms in Singapore were referenced in the study. They were golden, oyster, shiitake and white button mushrooms, as well as dried and canned mushrooms. However, it is likely that other mushrooms not referenced would also have beneficial effects.

The researchers believe the reason for the reduced prevalence of MCI in mushroom eaters may be down to a specific compound found in almost all varieties. “We’re very interested in a compound called ergothioneine (ET),” said Dr. Irwin Cheah, Senior Research Fellow at the NUS Department of Biochemistry. “ET is a unique antioxidant and anti-inflammatory which humans are unable to synthesise on their own. But it can be obtained from dietary sources, one of the main ones being mushrooms.”

An earlier study by the team on elderly Singaporeans revealed that plasma levels of ET in participants with MCI were significantly lower than age-matched healthy individuals. The work, which was published in the journal Biochemical and Biophysical Research Communications in 2016, led to the belief that a deficiency in ET may be a risk factor for neurodegeneration, and increasing ET intake through mushroom consumption might possibly promote cognitive health.

Other compounds contained within mushrooms may also be advantageous for decreasing the risk of cognitive decline. Certain hericenones, erinacines, scabronines and dictyophorines may promote the synthesis of nerve growth factors. Bioactive compounds in mushrooms may also protect the brain from neurodegeneration by inhibiting production of beta amyloid and phosphorylated tau, and acetylcholinesterase.

Next steps

The potential next stage of research for the team is to perform a randomised controlled trial with the pure compound of ET and other plant-based ingredients, such as L-theanine and catechins from tea leaves, to determine the efficacy of such phytonutrients in delaying cognitive decline. Such interventional studies will lead to more robust conclusion on causal relationship. In addition, Asst Prof Feng and his team also hope to identify other dietary factors that could be associated with healthy brain ageing and reduced risk of age-related conditions in the future.

https://medicalxpress.com/news/2019-03-mushrooms-cognitive-decline.html

BY ARIS FOLLEY

A Texas man is planning to spend his retirement years at Holiday Inns nationwide instead of moving into a nursing home, in an effort to cut costs, ABC affiliate WSET reported. Terry Robinson of Spring, Texas, listed his reasons for spending his golden years as a customer of the hotel chain in a viral post on Facebook earlier this month.

While the average cost of a nursing home can amount to $188.00 per day, Robinson wrote in the post that reservations at the Holiday Inn cost $59.23 per night with a “combined long term stay discount and senior discount.”

“Breakfast is included and some have happy hours in the afternoon,” Robinson wrote. “That leaves $128.77 a day for lunch and dinner in any restaurant we want, or room service, laundry, gratuities and special TV movies. Plus, they provide a spa, swimming pool, a workout room, a lounge and washer-dryer, etc.”

“Most have free toothpaste and razors, and all have free shampoo and soap,” he went on to write, adding that “$5 worth of tips a day and you’ll have the entire staff scrambling to help you.”

“They treat you like a customer, not a patient,” he said.

Robinson added that the staff will also “call an ambulance … or the undertaker” if anything bad happens. Robinson also said that he would be able to travel wherever he wants with the retirement plan, as the Holiday Inn has more than 1,100 locations accords the world, according to USA Today. As for family visits, Robinson wrote that “they will always be glad to find you, and probably check in for a few days mini-vacation.”

“The grand-kids can use the pool,” he added.

Robinson’s post has gone on to rack up more than 108,000 shares as of Tuesday. According to CNBC, the annual expense of a private room in a nursing home hit the six-figure threshold as of October 2018. Nursing home care is typically meant for people who are not self-sufficient and involves assistance by trained medical staff. The report found in a new study that the national annual median cost of a private room in a nursing home amounted to roughly $100,375. The most expensive place for care in a nursing home in the United States was Alaska, according to the study, where the annual median cost of a room in a nursing home was reportedly $330,873. Washington, D.C., reportedly has the highest cost for a one-bedroom at an assisted living facility, with the annual median cost estimated to be about $111,195.

https://thehill.com/blogs/blog-briefing-room/news/431576-man-goes-viral-with-plan-to-retire-to-a-holiday-inn-instead-of