Posts Tagged ‘aging’

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

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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

by CHRISTIAN COTRONEO

If the startling results of a recent Austrian study are any indication, we should all get better acquainted with ashitaba.

In fact, we might even want to make a little room for this ancient Japanese plant beside the basil and lavender in the windowsill.

Ashitaba may have a bright future in Western households because the so-called “Tomorrow’s Leaf” promises just that: A future.

In a paper published this month in the journal Nature, researchers at the University of Graz, suggest a key component of the plant — called 4,4′-dimethoxychalcone, or DMC — may act as an anti-aging mechanism.

In experiments, the substance was found to prolong the lives of worms and fruit flies by as much as 20 percent.

Keeping the cellular process tidy
Researchers suggest DMC acts as a kind of “cellular garbage collector.” It basically speeds along the natural process by which frail and damaged cells are shed to be replaced by shiny new ones.

Normally, the crusty old cells are removed regularly through a process called autophagy. But as we age, the body’s trash collector starts missing appointments, allowing the damaged cells to accumulate, opening the door for a wide range of diseases and disorders.

In the experiments, DMC kept the process whirring along.

So what exactly is this humble hero — and more importantly, why haven’t we carpeted the planet with it yet?

Well, it’s not much to look at, and its leaves are said to be rather bitter — but that likely just gives adds more cred for its centuries-long use as a traditional medicine.

Let’s face it, practitioners of traditional medicine were probably the first to offer the cheerful slogan, “It tastes awful and it works.”

And those ancient chemists stood by the myriad benefits of Angelica keiskei — the plant’s botanical name — touting its powers of increasing breast milk flow, easing blood pressure and even calming the savage ulcer.

Samurai, too, were notorious nibblers— not so much for the plant’s breast milk-boosting ways, but rather its reputation for adding years to one’s life.

But does it really work? Or does it get a pass from traditional medicine because it tastes awful?

Keep in mind that Austrian researchers developed an intensive process to isolate the DMC, administering concentrated dosages to subjects. You’re not likely to be overwhelm your anti-aging genes by chewing on a bale of ashitaba, or making it into a nice tea.

Also, although this was the first time DMC was tested on living animals, there’s a wide chasm between worms and human beings. Countless promising experiments involving animals have crashed hard against the very different reality of human biology.

“The experiments indicate that the effects of DMC might be transferable to humans, although we have to be cautious and wait for real clinical trials,” Frank Madeo, lead author of the study, tells Medical News Today.

Human testing, he adds, will follow, only after researchers see how DMC fares at torquing the hearts of mice.

Of course, that doesn’t mean you can’t get a headstart on what could well become the ultimate opiate for the age-obsessed masses — and grow your own little ashitaba garden.

“Angelicas [another name for the plant] like to be cold stratified,” San Francisco Botanical Garden curator Don Mahoney tells Modern Farmer.

That means keeping the seeds outside at night, preferably in 30-degree temperatures, to help them germinate. As an alternative, Mahoney suggests, a couple of weeks in the fridge could kickstart the process.

“Nearly all of my last batch of seeds germinated,” he explains.

From there, it’s all in the hands of quality soil, while you gradually increase the pot size until the seedling are ready for the ground.

Ashitaba is partial to cool, damp conditions. So in the summer, it might seem like you messed up yet another gardening gambit. But then, when things cool down, “Tomorrow’s Leaf” rises mightily to the occasion.

The plants generally grow to around four feet high. Not only that, but they have a remarkable knack for rejuvenating themselves — a leaf cut off in the morning will start growing back the next day.

As far as looks go, ashitaba, which is a relative of the carrot, isn’t going to make your begonias blush. But its leaves, stems and yellow sap still course with nutrients. Even if the age-torquing upside doesn’t work out, it still packs promise for ulcers and breast milk and even blood pressure.

At the very least, all that promise of extending life will be a nice conversation piece — even if all it ever ends up enlivening is your salad.

And remember: Even the samurai died of old age at some point.

https://www.mnn.com/your-home/organic-farming-gardening/stories/ashitaba-plant-antiaging-properties-how-to-grow

By Alejandra Viviescas

A higher level of education is not related to better cognitive reserve — the ability of the adult brain to maintain normal cognitive function in the presence of neurodegeneration — in old age, a study suggests. However, the study, titled “Education and cognitive reserve in old age,” did find that it allowed people to store more information before reaching old age. It was published in the journal Neurology.

Higher education levels are widely associated with a higher cognitive reserve, lower risk of dementia, and delayed cognitive decline — the reduced storage capacity in the brain that usually occurs as a person ages. However, scientific evidence supporting these claims is controversial. Some studies suggest that this association is mostly due to the connection between education and a higher acquisition of knowledge rather than higher adaptability.

To assess the contribution of education to cognitive reserve in old age, researchers from Rush University in Chicago analyzed 2,899 participants (older than 50 years of age; average age of 77.8 years) who participated in two ongoing clinical studies: the Religious Orders Study, which began in 1994 and included older Catholic clergy members from across the U.S.; and the Memory and Aging Project, which began in 1997 and involved older laypeople from the Chicago metropolitan region.

At the time of enrollment, none of the participants had been diagnosed with dementia.

They were followed for an average of eight years; 2,143 (73.9%) were women, and 2,569 (88.6%) were white. All participants took cognitive tests once a year, and data were collected between 1994 and 2018.

Researchers evaluated two subgroups, the first one — the incident dementia subgroup — consisted of 696 participants who developed incident dementia during follow-up over a mean of 10.5 years. The second one — the incident dementia neuropathologically examined subgroup — included 405 individuals who died during follow-up and underwent an autopsy to assess if they had any neurodegenerative conditions.

Participants had a mean of 16.3 years of education, ranging from zero to 30. Higher education was associated with an initial higher rate of global cognition at a younger age but not with more significant cognitive change. This means that more educated people had a high storage capacity at the beginning of the study, but did not show greater cognitive adaptability.

There was a quicker decline in cognition in patients who developed dementia about 1.8 years before diagnosis. The level of education did not alter this decrease.

In the patients who had died, there was a faster cognition decline approximately 3.4 years before death. The level of education did not alter this decline, but researchers noted that in individuals with higher education, this decline started about 0.2 years earlier.

People with higher education were less likely to have areas of dead tissue in the brain. “There have been previous reports linking higher level of education with a lower risk of stroke consistent with the present findings,” according to the researchers. Higher education was not associated with any other neuropathology.

“The results suggest that the contribution of education to cognitive reserve is limited to its association with premorbid cognitive level and does not involve an association with cognitive aging trajectories,” the researchers wrote.

“That education apparently contributes little to cognitive reserve is surprising given its association with cognitive growth and changes in brain structure. However, formal education typically ends decades before old age begins … This implies that influences on cognitive reserve vary over time, with recent experiences more influential than remote experiences such as schooling,” they added.

The researchers noted that most individuals had some level of education, which might underestimate the effects on a non-educated group. Therefore, further studies that evaluate a higher sample of participants with less education would help them better understand the association between education and cognition.

https://alzheimersnewstoday.com/2019/02/13/education-brain-adaptability-old-age/

The discovery sheds new light on the origins of this most common cause of dementia, a hallmark of which is the buildup of tangled tau protein filaments in the brain.

The finding could also lead to new treatments for Alzheimer’s and other diseases that progressively destroy brain tissue, conclude the researchers in a paper about their work that now features in the journal Neuron.

Scientists from Massachusetts General Hospital (MGH) in Charlestown and the Johns Hopkins School of Medicine in Baltimore, MD, led the study, which set out to investigate how tau protein might contribute to brain cell damage.

Alzheimer’s disease does not go away and gets worse over time. It is the sixth most common cause of death in adults in the United States, where an estimated 5.7 million people have the disease.

Exact causes of Alzheimer’s still unknown

Exactly what causes Alzheimer’s and other forms of dementia is still a mystery to science. Evidence suggests that a combination of environment, genes, and lifestyle is involved, with different factors having different amounts of influence in different people.

Most cases of Alzheimer’s do not show symptoms until people are in their 60s and older. The risk of getting the disease rises rapidly with age after this.

Brain studies of people with the disease — together with postmortem analyses of brain tissue — have revealed much about how Alzheimer’s changes and harms the brain.

“Age-related changes” include: inflammation; shrinkage in some brain regions; creation of unstable, short-lived molecules known as free radicals; and disruption of cellular energy production.

The brain of a person with Alzheimer’s disease also has two distinguishing features: plaques of amyloid protein that form between cells, and tangles of tau protein that form inside cells. The recent study concerns the latter.

Changes to tau behavior

Brain cells, or neurons, have internal structures known as microtubules that support the cell and its function. They are highly active cell components that help carry substances from the body of the cell out to the parts that connect it to other cells.

In healthy brain cells, tau protein normally “binds to and stabilizes” the microtubules. Tau behaves differently, however, in Alzheimer’s disease.

Changes in brain chemistry make tau protein molecules come away from the microtubules and stick to each other instead.

Eventually, the detached tau molecules form long filaments, or neurofibrillary tangles, that disrupt the brain cell’s ability to communicate with other cells.

The new study introduces the possibility that, in Alzheimer’s disease, tau disrupts yet another mechanism that involves communication between the nucleus of the brain cell and its body.

Communication with cell nucleus

The cell nucleus communicates with the rest of the cell using structures called nuclear pores, which comprise more than 400 different proteins and control the movement of molecules.

Studies on the causes of amyotrophic lateral sclerosis, frontotemporal, and other types of dementia have suggested that flaws in these nuclear pores are involved somehow.

The recent study reveals that animal and human cells with Alzheimer’s disease have faulty nuclear pores, and that the fault is linked to tau accumulation in the brain cell.

“Under disease conditions,” explains co-senior study author Bradley T. Hyman, the director of the Alzheimer’s Unit at MGH, “it appears that tau interacts with the nuclear pore and changes its properties.”

He and his colleagues discovered that the presence of tau disrupts the orderly structure of nuclear pores containing the major structural protein Nup98. In Alzheimer’s disease cells, there were fewer of these pores and those that were there tended to be stuck to each other.

‘Mislocalized’ Nup98
They also observed another curious change involving Nup98 inside Alzheimer’s disease brain cells. In cells with aggregated tau, the Nup98 was “mislocalized” instead of staying in the nuclear pore.

They revealed that this feature was more exaggerated in brain tissue of people who had died with more extreme forms of Alzheimer’s disease.

Finally, when they added human tau to living cultures of rodent brain cells, the researchers found that it caused mislocalization of Nup98 in the cell body and disrupted the transport of molecules into the nucleus.

This was evidence of a “functional link” between the presence of tau protein and damage to the nuclear transport mechanism.

The authors note, however, that it is not clear whether the Nup98-tau interaction uncovered in the study just occurs because of disease or whether it is a normal mechanism that behaves in an extreme fashion under disease conditions.

They conclude:

“Taken together, our data provide an unconventional mechanism for tau-induced neurodegeneration.”

https://www.medicalnewstoday.com/articles/322991.php

machine-learning-model-provides-early-dementia-diagnosis-306451

A machine learning-based model using data routinely gathered in primary care identified patients with dementia in such settings, according to research recently published in BJGP Open.

“Improving dementia care through increased and timely diagnosis is a priority, yet almost half of those living with dementia do not receive a timely diagnosis,” Emmanuel A. Jammeh, PhD, of the science and engineering department at Plymouth University in the United Kingdom, and colleagues wrote.

“A cost-effective tool that can be used by [primary care providers] to identify patients likely to be living with dementia, based only on routine data would be extremely useful. Such a tool could be used to select high-risk patients who could be invited for targeted screening,” they added.

The researchers used Read codes, a set of clinical terms used in the U.K. to summarize data for general practice, to develop a machine learning-based model to identify patients with dementia. The Read codes were selected based on their significant association with patients with dementia, and included codes for risk factors, symptoms and behaviors that are collected in primary care. To test the model, researchers collected Read-encoded data from 26,483 patients living in England aged 65 years and older.

Jammeh and colleagues found that their machine-based model achieved a sensitivity of 84.47% and a specificity of 86.67% for identifying dementia.

“This is the first demonstration of a machine-learning approach to identifying dementia using routinely collected [National Health Service] data, researchers wrote.

“With the expected growth in dementia prevalence, the number of specialist memory clinics may be insufficient to meet the expected demand for diagnosis. Furthermore, although current ‘gold standards’ in dementia diagnosis may be effective, they involve the use of expensive neuroimaging (for example, positron emission tomography scans) and time-consuming neuropsychological assessments which is not ideal for routine screening of dementia,” they continued.

The model will be evaluated with other datasets, and have its validation tested “more extensively” at general practitioner practices in the future, Jammeh and colleagues added. – by Janel Miller

https://www.healio.com/family-medicine/geriatric-medicine/news/online/%7B62392171-6ad7-481a-9289-bd69df49d4a4%7D/machine-learning-based-model-may-identify-dementia-in-primary-care