Posts Tagged ‘dementia’

According to the results of a study published in Nature, gaming could possibly increase the volume of gray matter in the brain.
Researchers recently studied the insular cortex regions of frequent gamers and those who didn’t play video games as regularly.
The study found a correlation between playing action video games and increased gray matter volume in the brain.

Do you ever feel you could do with polishing up on your cognitive skills?

Well, according to the results of a study published in Nature, gaming could possibly be the way forward.

Researchers from the Chinese University of Electronic Science and Technology and the Australian Macquarie University in Sydney joined forces, and recently found a correlation between playing action video games and increased gray matter volume in the brain.

How video games stimulate the gray matter in your brain

The focus of the team’s research was on the insular cortex, a part of the cerebral cortex folded deep in the brain that has been the subject of very few studies to date.

It’s thought that a large part of linguistic processing takes place in this region of the brain, and that other processes relating to taste and smell, compassion and empathy, and interpersonal experiences are also managed here.

The study looked at 27 regular video game players described in the study as “Action Video Game experts” as well as 30 amateurs who played less frequently and didn’t perform as well in games.

The participants in the “expert” group were all recognised participants of regional or national championships of League of Legends and Dota 2. Using an MRI scanner, the scientists took detailed pictures of the participants’ insular cortices.

“By comparing AVG experts and amateurs, we found that AVG experts had enhanced functional connectivity and gray matter volume in insular subregions,” wrote the research team.

Gaming actually promotes networking within the brain

The gray matter in your brain is part of your central nervous system and essentially controls all your brain’s functions.

It follows that better connectivity in this region will lead to faster thought processes and correspondingly higher intelligence.

If you want to improve your cognitive performance, you don’t necessarily have to resort to hours of video games; sports and art-based recreation are just two among many activities that promote connectivity in the brain.

However it does mean that those who still like to sit in front of their console from time to time no longer need to feel guilty about being sat in front of a screen — after all, it is exercise — just for the brain.

https://www.businessinsider.com/video-games-may-increase-your-brains-gray-matter-2018-12

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By Ana Sandoiu

New research finds that a 6-month regimen of aerobic exercise can reverse symptoms of mild cognitive impairment in older adults.

Mild cognitive impairment (MCI) is characterized by a mild loss of cognitive abilities, such as memory and reasoning skills.

A person with MCI may find it hard to remember things, make decisions, or focus on tasks.

While the loss of cognitive abilities is not serious enough to interfere with daily activities, MCI raises the risk of Alzheimer’s disease and other forms of dementia.

According to the Alzheimer’s Association, 15–20 percent of adults aged 65 and over in the United States have MCI.

New research suggests that there might be a way to reverse these age-related cognitive problems. James A. Blumenthal, Ph.D. — of Duke University Medical Center in Durham, NC — and colleagues examined the effects of regimented exercise in 160 people aged 65 on average.

They published their findings in the journal Neurology.


A normal brain of a 70-year-old (left slice), compared with the brain of a 70-year-old with Alzheimer’s disease.Credit: Jessica Wilson/Science Photo Library

Neuroscientists have amassed more evidence for the hypothesis that sticky proteins that are a hallmark of neurodegenerative diseases can be transferred between people under particular conditions — and cause new damage in a recipient’s brain.

They stress that their research does not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

“The risk may turn out to be minor — but it needs to be investigated urgently,” says John Collinge, a neurologist at University College London who led the research, which is published in Nature1 on 13 December.

The work follows up on a provocative study published by Collinge’s team in 20152. The researchers discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. Collinge and his colleagues suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Seeds of trouble
Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and they cause local bleeding. In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

The team has now more directly tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. Britain stopped the cadaver-derived growth hormone treatment in 1985 and replaced it with a treatment that uses synthetic growth hormone. But Collinge’s team was able to locate old batches of the growth-hormone preparation stored as powder for decades at room temperature in laboratories at Porton Down, a national public-health research complex in southern England.

When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests
To test whether the amyloid-beta in these batches could cause the amyloid pathology, they injected samples directly into the brains of young mice genetically engineered to be susceptible to amyloid pathology. By mid-life, the mice had developed extensive amyloid plaques and CAA. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

The scientists are now checking in separate mouse experiments whether the same is true for the tau protein.

“It’s an important study, though the results are very expected,” says Mathias Jucker at the Hertie Institute for Clinical Brain Research in Tubingen, Germany. Jucker demonstrated in 2006 that amyloid-beta extracted from human brain could initiate CAA and plaques in the brains of mice3. Many other mouse studies have also since confirmed this.

Surgical implications
That the transmissibility of the amyloid-beta could be preserved after so many decades underlines the need for caution, says Jucker. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods4. But Jucker also notes that, because degenerative diseases take a long time to develop, the danger of any transfer may be most relevant in the case of childhood surgery where instruments have also been used on old people.

So far, epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life — because medical databases tend not to include this type of data.

But epidemiologist Roy Anderson at Imperial College London says researchers are taking the possibility seriously. Major population cohort studies, such as the US Framingham Heart Study, are starting to collect information about participants’ past surgical procedures, along with other medical data.

The 2015 revelation prompted pathologists around the world to reexamine their own cases of people who had been treated with similar growth-hormone preparations — as well as people who had acquired CJD after brain surgery that had involved the use of contaminated donor brain membranes as repair patches. Many of the archived brain specimens, they discovered, were full of aberrant amyloid plaques5,6,7. One study showed that some batches of growth-hormone preparation used in France in the 1970s and 1980s were contaminated with amyloid-beta and tau — and that tau was also present in three of their 24 patients.8

Collinge says he applied unsuccessfully for a grant to develop decontamination techniques for surgical instruments after his 2015 paper came out. “We raised an important public-health question, and it is frustrating that it has not yet been addressed.” But he notes that an actual risk from neurosurgery has not yet been established.

https://www.nature.com/articles/d41586-018-07735-w?utm_source=fbk_nnc&utm_medium=social&utm_campaign=naturenews&sf204283628=1

Thank to Kebmodee for bringing this to the It’s Interesting community.

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High school students in 1960 take the Project Talent test, the largest survey of American teenagers ever done; it is now being used for research into dementia. (American Institutes for Research)

By Tara Bahrampour

In 1960, Joan Levin, 15, took a test that turned out to be the largest survey of American teenagers ever conducted. It took two-and-a-half days to administer and included 440,000 students from 1,353 public, private and parochial high schools across the country — including Parkville Senior High School in Parkville, Md., where she was a student.

“We knew at the time that they were going to follow up for a long time,” Levin said — but she thought that meant about 20 years.

Fifty-eight years later, the answers she and her peers gave are still being used by researchers — most recently in the fight against Alzheimer’s disease. A study released this month found that subjects who did well on test questions as teenagers had a lower incidence of Alzheimer’s and related dementias in their 60s and 70s than those who scored poorly.

Known as Project Talent, the test was funded by the U.S. government, which had been concerned, given the Soviet Union’s then-recent successful Sputnik launch, that Americans were falling behind in the space race.

Students answered questions about academics and general knowledge, as well as their home lives, health, aspirations and personality traits. The test was intended to identify students with aptitudes for science and engineering. Test-takers included future rock stars Janis Joplin, then a senior at Thomas Jefferson High School in Port Arthur, Tex., and Jim Morrison, then a junior at George Washington High School in Alexandria, Va.

In recent years, researchers have used Project Talent data for follow-up studies, including one published Sept. 7 in the Journal of the American Medical Association. Conducted by researchers at the Washington-based American Institutes for Research (AIR), the organization that originally administered the test, it compared results for more than 85,000 test-takers with their 2012-2013 Medicare claims and expenditures data, and found that warning signs for dementia may be discernible as early as adolescence.

The study looked at how students scored on 17 areas of cognitive ability such as language, abstract reasoning, math, clerical skills, and visual and spatial prowess, and found that people with lower scores as teenagers were more prone to getting Alzheimer’s and related dementias in their 60s and early 70s.

Specifically, those with lower mechanical reasoning and memory for words as teens had a higher likelihood of developing dementia in later life: Men in the lower-scoring half were 17 percent more likely, while women with lower scores were 16 percent more likely. Worse performance on other components of the test also increased the risk for later-life dementia.

An estimated 5.7 million Americans have Alzheimer’s disease, and in the absence of scientific breakthroughs to curb the disease, the Alzheimer’s Association projects that number could reach 14 million by 2050, with the cost of care topping $1 trillion per year.

The 1960 test could have the potential to be like the groundbreaking Framingham study, a decades-long study of men in Massachusetts that led to reductions in heart disease in the 1970s, ’80s and ’90s, said Susan Lapham, director of Project Talent and a co-author of the JAMA study.

“If Project Talent can be for dementia what the Framingham study was for heart disease, it will make a difference in public health,” she said. “It indicates that we should be designing interventions for kids in high school and maybe even earlier to maybe keep their brains active from a young age.”

This might include testing children, identifying those with lower scores and “getting them into a program to make sure they’re not missing out and maybe putting themselves at risk,” she said.

For years, little was done with the Project Talent data because the participants could not be found. A proposal in the 1980s to try to find them failed because, in that pre-Internet age, the task seemed too daunting.

In 2009, as the students’ 50th high school reunions were coming up, researchers decided to use the gatherings as an occasion to contact many of them. (About a quarter have died.) They were then able to use the test data to study things such as the effects of diabetes and personality type on later-life health.

But when contacted, the participants were most interested in dementia, Lapham said. “They wanted that to be studied more than any other topic,” she said. “They said, ‘The thing I fear most is dementia.’ ”

While students were supposed to have received their results soon after taking the test, some students said they did not remember getting them.

Receiving her results recently was interesting in hindsight, said Levin, a retired human-resources director who is now 73 and living in Cockeysville, Md. Most of her scores were over 75 percent, with very high marks in vocabulary, abstract reasoning and verbal memory, and lower marks in table reading and clerical tasks.

Low scores do not mean a person will get dementia; the correlation is merely associated with a higher risk. But even if her scores had been lower, Levin said she would want to know. “I’m kind of a planner, and I look ahead,” she said. “I’d want my daughter and her family to maybe have an idea of what to expect.”

Karen Altpeter, 75, of Prescott, Wis., said she would also probably want to know about her risk, because her mother and grandmother had Alzheimer’s. She liked the idea that the answers she had given as a teen could help science.

“If there’s any opportunity I can have to make a difference just by taking a test and answering some questions, I’ll do it,” she said. “I want the opportunity to make things better for people.”

Earlier studies had suggested a relationship between cognitive abilities in youth and dementia in later life, including one that followed 800 nuns earlier in the 20th century and found that the complexity of sentences they used in writing personal essays at 21 correlated with their dementia risk in old age.

But that study included only women and no minorities. Project Talent’s subjects reflected the nation’s demographic mix in 1960.

Today, however, the country is more diverse. The number of minorities 65 and older is projected to grow faster than the general population, and by 2060 there will be about 3.2 million Hispanics and 2.2 million African Americans with Alzheimer’s disease and related dementias, according to a study by the Centers for Disease Control and Prevention published this week. African Americans and Hispanics have a higher prevalence of Alzheimer’s and related diseases than non-Hispanic whites.

A follow-up study underway of a smaller sample of the Project Talent pool — 22,500 people — will be weighted to reflect today’s population mix and will dig more deeply into age-related brain and cognitive changes over time.

It will examine the long-term impact of school quality and school segregation on brain health, and the impact of adolescent socioeconomic disadvantage on cognitive and psychosocial resilience, with a special focus on the experiences of participants of color.

That study includes an on-paper survey of demographics, family and marriage history, residential history, educational attainment and health status; an online survey of health, mental health and quality of life; and a detailed cognitive assessment by phone of things such as memory for words and counting backward.

Researchers will also evaluate school quality to determine whether there are racial or ethnic differences in the benefits of attending higher quality schools, and explore more deeply why some people develop dementia and some do not.

The follow-up, slated to be completed next year, is funded by the National Institute on Aging, part of the National Institutes of Health, and conducted by AIR in conjunction with researchers from Columbia University Medical Center and the University of Southern California.

Cliff Jacobs, 75, of Arlington, Va., who took the Project Talent test as a high school junior in Tenafly, N.J., doesn’t remember hearing about any results. Then, a few months ago, researchers conducting the follow-up study contacted him, tested his cognitive abilities and asked about his life history.

“They delved into my issues growing up — did my parents smoke, and was I exposed to any secondhand smoke? Yeah, my parents both smoked, and I didn’t even think it was something to consider,” he said.

A retired geoscientist for the National Science Foundation, Jacobs said he would be interested in learning if he is at risk for dementia.

“The statistical correlation is not one that will necessarily apply to you, but they can give you some probabilities,” he said. “I guess basic human nature would be, ‘Yeah, you’d probably want to know.’ ”

Try these 12 sample questions from the test.


Can’t see the Quiz? Click Here.

1

In the Bible story, Samson knew he would lose his strength if

his hair were cut.

he fell in love.

he left Jerusalem.

he spoke with a Philistine.

he went to war.

2

Chartreuse is a mixture of

green and blue.

yellow and orange.

yellow and green.

orange and brown.

red and orange.

3

The above is usually called a

fly.

spoon.

spinner.

plug.

streamer.

4

High pointed arches are used chiefly in

Roman architecture.

Greek architecture.

Gothic architecture.

Renaissance architecture.

modern architecture.

5

If a camper sees a garter snake, he should

leave it alone.

pin its head down with a forked stick.

hit it with a rock.

climb the nearest tree.

stand still until it leaves.

6

Tartar sauce is most often served with

tossed salad.

ice cream.

fish.

barbecued beef.

chow mein.

7

Suppose that after the post office is closed, someone finds he urgently needs stamps. He should probably try getting them

in a drug store.

from a stamp collector.

by phoning the postmaster’s home.

in a department store.

in a gas station.

8

In a suspension bridge, the road bed is supported by

pontoons.

pilings.

arches.

cables.

cantilevers.

9

Which of these guns has the largest bore?

12 ga.

.22 cal.

.44 cal.

16 ga.

20 ga.

10

A boy takes a girl to a movie and they find a pair of seats on a side aisle. Usually the girl should take the seat

on the left.

on the right.

nearest the aisle.

furthest from the aisle.

nearest the center of the theater.

11

About when did Leonardo de Vinci live?

1st century

5th century

10th century

15th century

20th century

12

Locks were built into the Panama Canal because

the Atlantic Ocean is higher than the Pacific.

the Pacific Ocean is higher than the Atlantic.

Panama is above sea level.

the canal is narrow.

the canal is wide.

germ_custom-ce83850a07c80ed6e717ea56370b3c5140eb2f3f-s800-c85

by BRET STETKA

Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer’s disease, the most common form of dementia worldwide, caused by a germ?

By “germ” he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer’s is infectious.

It’s an idea that just a few years ago would’ve seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer’s research for years, but until very recently not much of it went toward investigating infection in causing dementia.

But this “germ theory” of Alzheimer’s, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.

If the germ theory gets traction, even in some Alzheimer’s patients, it could trigger a seismic shift in how doctors understand and treat the disease.

For instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it’s worth looking into.

Norins received his medical degree from Duke in the early 1960s, and after a stint at the Centers for Disease Control and Prevention he fell into a lucrative career in medical publishing. He eventually settled in an admittedly aged community in Naples, Fla., where he took an interest in dementia and began reading up on the condition.

After scouring the medical literature he noticed a pattern.

“It appeared that many of the reported characteristics of Alzheimer’s disease were compatible with an infectious process,” Norins tells NPR. “I thought for sure this must have already been investigated, because millions and millions of dollars have been spent on Alzheimer’s research.”

But aside from scattered interest through the decades, this wasn’t the case.

In 2017, Norins launched Alzheimer’s Germ Quest Inc., a public benefit corporation he hopes will drive interest into the germ theory of Alzheimer’s, and through which his prize will be distributed. A white paper he penned for the site reads: “From a two-year review of the scientific literature, I believe it’s now clear that just one germ — identity not yet specified, and possibly not yet discovered — causes most AD. I’m calling it the ‘Alzheimer’s Germ.’ ”

Norins is quick to cite sources and studies supporting his claim, among them a 2010 study published in the Journal of Neurosurgery showing that neurosurgeons die from Alzheimer’s at a nearly 2 1/2 times higher rate than they do from other disorders.

Another study from that same year, published in The Journal of the American Geriatric Society, found that people whose spouses have dementia are at a 1.6 times greater risk for the condition themselves.

Contagion does come to mind. And Norins isn’t alone in his thinking.

In 2016, 32 researchers from universities around the world signed an editorial in the Journal of Alzheimer’s Disease calling for “further research on the role of infectious agents in [Alzheimer’s] causation.” Based on much of the same evidence Norins encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer’s are now justified.

NPR reported on an intriguing study published in Neuron in June that suggested that viral infection can influence the progression of Alzheimer’s. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with that affected by dementia.

But something kept getting in the way: herpes.

Dudley’s team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).

Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as shingles, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.

But having the herpes viruses alone doesn’t mean inevitable brain decline. After all, up to 75 percent of us may harbor HHV-6 .

But Dudley also noticed that herpes appeared to interact with human genes known to increase Alzheimer’s risk. Perhaps, he says, there is some toxic combination of genetic and infectious influence that results in the disease; a combination that sparks what some feel is the main contributor to the disease, an overactive immune system.

The hallmark pathology of Alzheimer’s is accumulation of a protein called amyloid in the brain. Many researchers have assumed these aggregates, or plaques, are simply a byproduct of some other process at the core of the disease. Other scientists posit that the protein itself contributes to the condition in some way.

The theory that amyloid is the root cause of Alzheimer’s is losing steam. But the protein may still contribute to the disease, even if it winds up being deemed infectious.

Work by Harvard neuroscientist Rudolph Tanzi suggests it might be a bit of both. Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube, and also in mice. He now believes the protein is part of our ancient immune system that like antibodies, ramps up its activity to help fend off unwanted bugs.

So does that mean that the microbe is the cause of Alzheimer’s, and amyloid a harmless reaction to it? According to Tanzi it’s not that simple.

Tanzi believes that in many cases of Alzheimer’s, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, called tau, to form tangles, which further harm brain cells.

But as Tanzi explains, the ultimate neurological insult in Alzheimer’s is the body’s reaction to this neurotoxic mess. All the excess protein revs up the immune system, causing inflammation — and it’s this inflammation that does the most damage to the Alzheimer’s-afflicted brain.

So what does this say about the future of treatment? Possibly a lot. Tanzi envisions a day when people are screened at, say, 50 years old. “If their brains are riddled with too much amyloid,” he says, “we knock it down a bit with antiviral medications. It’s just like how you are prescribed preventative drugs if your cholesterol is too high.”

Tanzi feels that microbes are just one possible seed for the complex pathology behind Alzheimer’s. Genetics may also play a role, as certain genes produce a type of amyloid more prone to clumping up. He also feels environmental factors like pollution might contribute.

Dr. James Burke, professor of medicine and psychiatry at Duke University’s Alzheimer’s Disease Research Center, isn’t willing to abandon the amyloid theory altogether, but agrees it’s time for the field to move on. “There may be many roads to developing Alzheimer’s disease and it would be shortsighted to focus just on amyloid and tau,” he says. “A million-dollar prize is attention- getting, but the reward for identifying a treatable target to delay or prevent Alzheimer’s disease is invaluable.”

Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit an at-risk brain. The vast majority of Alzheimer’s treatment trials have failed, including many targeting amyloid. But it could be that the patients included were too far along in their disease to reap any therapeutic benefit.

If a microbe is responsible for all or some cases of Alzheimer’s, perhaps future treatments or preventive approaches will prevent toxin protein buildup in the first place. Both Tanzi and Norins believe Alzheimer’s vaccines against viruses like herpes might one day become common practice.

In July of this year, in collaboration with Norins, the Infectious Diseases Society of America announced that they plan to offer two $50,000 grants supporting research into a microbial association with Alzheimer’s. According to Norins, this is the first acknowledgement by a leading infectious disease group that Alzheimer’s may be microbial in nature – or at least that it’s worth exploring.

“The important thing is not the amount of the money, which is a pittance compared with the $2 billion NIH spends on amyloid and tau research,” says Norins, “but rather the respectability and more mainstream status the grants confer on investigating of the infectious possibility. Remember when we thought ulcers were caused by stress?”

Ulcers, we now know, are caused by a germ.

https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest?ft=nprml&f=1001

by Wilson Jacob

Dementia screening is more effective in winter and spring because that’s when tell-tale proteins flare up, new research suggests.

In a large-scale study of elderly people in the US, France and Canada, researchers found cognitive ability of over-70s in general is much sharper in summer and fall.

Brain-wise, healthy subjects seemed on average 4.8 years younger during those months than they did between November and May.

Those with Alzheimer’s pathology also experienced ‘dips’ in the winter, due to ‘seasonal rhythms’ in certain proteins, which seemed to make dementia-related genes more expressed in the brain.

The findings suggest that assessing people for the neurodegenerative disease in the latest and earliest months of the year might be the most effective way to detect the disease, for which there is still no definitive test.

People with dementia experience ‘dips’ in winter due to ‘seasonal rhythms’ in Alzheimer’s-related proteins, which seems to make dementia genes more expressed in the brain

According to lead author Dr Andrew Lim, assistant professor of neurology at the University of Toronto, the findings are a significant step towards improving Alzheimer’s diagnosis and treatment.

‘This association was independent of mood, sleep, physical activity, and thyroid status,’ he explained.

‘It was clinically significant, as reflected in a nearly 30 percent higher odds of meeting criteria for mild cognitive impairment or dementia in winter and spring compared to summer and fall, and it persisted in cases with pathologically confirmed Alzheimer’s disease.’

He adds: ‘There may be value in increasing dementia-related clinical resources in the winter and early spring when symptoms are likely to be most pronounced.

‘By shedding light on the mechanisms underlying the seasonal improvement in cognition in the summer and early fall, these findings also open the door to new avenues of treatment for Alzheimer’s disease.’

Several studies suggested season may be associated with cognitive function in some populations of younger adults.

But studies of the seasonal impact in older adults was lacking and little known about the underlying mechanisms.

So 3,353 older adults over 70 with and without Alzheimer’s in three cohort studies in the United States, Canada, and France were recruited.

They tested their thinking and concentration, and the Alzheimer-disease-related proteins in their spinal fluid measured.

Autopsies on those who died were performed and the brain was measured.

The average cognitive functioning was higher in the summer and autumn than the winter and spring, equivalent in cognitive effect to 4.8 years difference in age-related decline.

In addition, the odds of meeting the diagnostic criteria for mild cognitive impairment or dementia were higher in the winter and spring than summer or autumn.

There are several theories as to what could be the cause for these piques and troughs.

First, Dr Lim explains, there are environmental factors like more light and warmer temperatures which could boost general cognition in the summer and fall.

‘If true, then interventions such as phototherapy or temperature modification may be effective in sustaining this peak year-round,’ he says.

Second, in the summer, we tend to be more active, with a better diet, and better sleeping habits.

‘In this study, the association between season and cognition was independent of self-reported sleep and physical activity, although studies incorporating objective markers of these and other behaviors may reveal a more important role for behavioral factors.’

Third, there is the ominous seasonal depressive disorder, which afflicts so many in the winter months. Those seasonal rhythms in psychological state, he says, may also drive the association between season and cognition.

‘In this study, the seasonality of cognition was independent of depression; however, other psychological factors, such as negative affect, which has been associated with mild cognitive impairment and dementia, may be important.’

Lastly, there are the things going on inside the body. All those factors – environmental, lifestyle and psychological – impact our hormone and vitamin levels.

‘In our study adjusting for serum levels of thyroid-stimulating hormone did not substantially attenuate estimates of the association between season and cognition,’ Dr Lim explains.

‘However, additional metabolic factors that may potentially link season to cognition are vitamin D, sex hormones like testosterone, and melatonin.’

The study, published today in the journal PLOS Medicine, had one clear limitation, among others: the participants were only assessed once a season, and only included data on individuals from temperate northern-hemisphere regions, not from southern-hemisphere or equatorial regions.

However, Dr Lim insists they are on to something.

‘The persistence of a robust summer/fall peak in cognition suggests that even in pathologically confirmed Alzheimer’s disease, there remains substantial cognitive plasticity.

‘Identifying drivers or mediators of this effect may enable leveraging this plasticity to improve cognition year-round.’

Dr Rosa Sancho, Head of Research of Alzheimer’s Research UK, concurred. The study is just one piece of the puzzle but sheds light on a rarely discussed element of the lives of dementia patients.

‘For most people with dementia, symptoms get steadily worse over the course of several years but there are things that can also impact memory and thinking ability in the short term. We know that factors like sleep quality and mood can affect cognitive performance whether or not someone has dementia, and this study suggests that the time of year may also influence these skills,’ she said.

https://www.habaricloud.today/2018/09/05/over-70s-cognition-skills-get-worse-during-cold-months-and-dementia-related-proteins-flare-up/

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