Posts Tagged ‘Alzheimer’s disease’

By Samiha Khanna

A quick eye exam might one day allow eye doctors to check up on both your eyeglasses prescription and your brain health.

A study of more than 200 people at the Duke Eye Center published March 11 in the journal Ophthalmology Retina suggests the loss of blood vessels in the retina could signal Alzheimer’s disease. Authors of the study include the Neurology Department’s James Burke, MD, PhD, and Cynthia Dunn, PA-C.

In people with healthy brains, microscopic blood vessels form a dense web at the back of the eye inside the retina, as seen in 133 participants in a control group.

In the eyes of 39 people with Alzheimer’s disease, that web was less dense and even sparse in places. The differences in density were statistically significant after researchers controlled for factors including age, sex, and level of education, said Duke ophthalmologist and retinal surgeon Sharon Fekrat, MD, the study’s senior author.

“We’re measuring blood vessels that can’t be seen during a regular eye exam and we’re doing that with relatively new noninvasive technology that takes high-resolution images of very small blood vessels within the retina in just a few minutes,” she said. “It’s possible that these changes in blood vessel density in the retina could mirror what’s going on in the tiny blood vessels in the brain, perhaps before we are able to detect any changes in cognition.”

The study found differences in the retinas of those with Alzheimer’s disease when compared to healthy people and to those with mild cognitive impairment, often a precursor to Alzheimer’s disease.

With nearly 6 million Americans living with Alzheimer’s disease and no viable treatments or noninvasive tools for early diagnosis, its burden on families and the economy is heavy. Scientists at Duke Eye Center and beyond have studied other changes in the retina that could signal trouble upstream in the brain, such as thinning of some of the retinal nerve layers.

“We know that there are changes that occur in the brain in the small blood vessels in people with Alzheimer’s disease, and because the retina is an extension of the brain, we wanted to investigate whether these changes could be detected in the retina using a new technology that is less invasive and easy to obtain,” said Dilraj S. Grewal, M.D., a Duke ophthalmologist and retinal surgeon and a lead author on the study. The Duke study used a noninvasive technology called optical coherence tomography angiography (OCTA). OCTA machines use light waves that reveal blood flow in every layer of the retina.

An OCTA scan could even reveal changes in tiny capillaries — most less than half the width of a human hair — before blood vessel changes show up on a brain scan such as an MRI or cerebral angiogram, which highlight only larger blood vessels. Such techniques to study the brain are invasive and costly.

“Ultimately, the goal would be to use this technology to detect Alzheimer’s early, before symptoms of memory loss are evident, and be able to monitor these changes over time in participants of clinical trials studying new Alzheimer’s treatments,” Fekrat said.

In addition to Fekrat and Grewal, study authors include Stephen P. Yoon, Atalie C. Thompson, Bryce W. Polascik, Cynthia Dunn and James R. Burke.

The research was supported by National Institutes of Health (P30EY005722), the 2018 Unrestricted Grant from Research to Prevent Blindness, and the Karen L. Wrenn Alzheimer’s Disease Award.

https://neurology.duke.edu/about/news/could-eye-doctor-diagnose-alzheimer%E2%80%99s-you-have-symptoms

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By Carl Zimmer

In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body.

Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease.

The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled.

A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions.

For some neuroscientists, new studies have changed the way they think about the brain.

One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.

“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”

He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.

Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too.

“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”

Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.

He hasn’t found those microbes, let alone that chemical. But “there’s something’s in there,” he said. “And we have to figure out what it is.”

‘It was considered crazy’

Scientists have long known that microbes live inside us. In 1683, the Dutch scientist Antonie van Leeuwenhoek put plaque from his teeth under a microscope and discovered tiny creatures swimming about.

But the microbiome has stubbornly resisted scientific discovery. For generations, microbiologists only studied the species that they could grow in the lab. Most of our interior occupants can’t survive in petri dishes.

In the early 2000s, however, the science of the microbiome took a sudden leap forward when researchers figured out how to sequence DNA from these microbes. Researchers initially used this new technology to examine how the microbiome influences parts of our bodies rife with bacteria, such as the gut and the skin.

Few of them gave much thought to the brain — there didn’t seem to be much point. The brain is shielded from microbial invasion by the so-called blood-brain barrier. Normally, only small molecules pass through.

“As recently as 2011, it was considered crazy to look for associations between the microbiome and behavior,” said Rob Knight, a microbiologist at the University of California, San Diego.

He and his colleagues discovered some of the earliest hints of these links. Investigators took stool from mice with a genetic mutation that caused them to eat a lot and put on weight. They transferred the stool to mice that had been raised germ-free — that is, entirely without gut microbiomes — since birth.

After receiving this so-called fecal transplant, the germ-free mice got hungry, too, and put on weight.

Altering appetite isn’t the only thing that the microbiome can do to the brain, it turns out. Dr. Cryan and his colleagues, for example, have found that mice without microbiomes become loners, preferring to stay away from fellow rodents.

The scientists eventually discovered changes in the brains of these antisocial mice. One region, called the amygdala, is important for processing social emotions. In germ-free mice, the neurons in the amygdala make unusual sets of proteins, changing the connections they make with other cells.

Studies of humans revealed some surprising patterns, too. Children with autism have unusual patterns of microbial species in their stool. Differences in the gut bacteria of people with a host of other brain-based conditions also have been reported.

But none of these associations proves cause and effect. Finding an unusual microbiome in people with Alzheimer’s doesn’t mean that the bacteria drive the disease. It could be the reverse: People with Alzheimer’s disease often change their eating habits, for example, and that switch might favor different species of gut microbes.

Fecal transplants can help pin down these links. In his research on Alzheimer’s, Dr. Sisodia and his colleagues transferred stool from ordinary mice into the mice they had treated with antibiotics. Once their microbiomes were restored, the antibiotic-treated mice started developing protein clumps again.

“We’re extremely confident that it’s the bacteria that’s driving this,” he said. Other researchers have taken these experiments a step further by using human fecal transplants.

If you hold a mouse by its tail, it normally wriggles in an effort to escape. If you give it a fecal transplant from humans with major depression, you get a completely different result: The mice give up sooner, simply hanging motionless.

As intriguing as this sort of research can be, it has a major limitation. Because researchers are transferring hundreds of bacterial species at once, the experiments can’t reveal which in particular are responsible for changing the brain.

Now researchers are pinpointing individual strains that seem to have an effect.

To study autism, Dr. Mauro Costa-Mattioli and his colleagues at the Baylor College of Medicine in Houston investigated different kinds of mice, each of which display some symptoms of autism. A mutation in a gene called SHANK3 can cause mice to groom themselves repetitively and avoid contact with other mice, for example.

In another mouse strain, Dr. Costa-Mattioli found that feeding mothers a high-fat diet makes it more likely their pups will behave this way.

by Debora MacKenzie

We may finally have found a long-elusive cause of Alzheimer’s disease: Porphyromonas gingivalis, the key bacteria in chronic gum disease. That’s bad, as gum disease affects around a third of all people. But the good news is that a drug that blocks the main toxins of P. gingivalis is entering major clinical trials this year, and research published this week shows it might stop and even reverse Alzheimer’s. There could even be a vaccine.

Alzheimer’s is one of the biggest mysteries in medicine. As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimer’s constitutes some 70 per cent of these cases and yet, we don’t know what causes it. The disease often involves the accumulation of proteins called amyloid and tau in the brain, and the leading hypothesis has been that the disease arises from defective control of these two proteins. But research in recent years has revealed that people can have amyloid plaques without having dementia. So many efforts to treat Alzheimer’s by moderating these proteins have failed, and the hypothesis has now been seriously questioned.

Indeed, evidence has been growing that the function of amyloid proteins may be as a defence against bacteria, leading to a spate of recent studies looking at bacteria in Alzheimer’s, particularly those that cause gum disease, which is known to be a major risk factor for the condition.

Bacteria involved in gum disease and other illnesses have been found after death in the brains of people who had Alzheimer’s, but until now, it hasn’t been clear whether these bacteria caused the disease or simply got in via brain damage caused by the condition.

Gum disease link

Multiple research teams have been investigating P. gingivalis, and have so far found that it invades and inflames brain regions affected by Alzheimer’s; that gum infections can worsen symptoms in mice genetically engineered to have Alzheimer’s; and that it can cause Alzheimer’s-like brain inflammation, neural damage, and amyloid plaques in healthy mice.

“When science converges from multiple independent laboratories like this, it is very compelling,” says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco, California.

In the new study, Cortexyme have now reported finding the toxic enzymes – called gingipains – that P. gingivalis uses to feed on human tissue in 96 per cent of the 54 Alzheimer’s brain samples they looked at, and found the bacteria themselves in all three Alzheimer’s brains whose DNA they examined.

“This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains, co-lococalising with plaques,” says Sim Singhrao, of the University of Central Lancashire, UK. Her team previously found that P. gingivalis actively invades the brains of mice with gum infections. She adds that the new study is also the first to show that gingipains slice up tau protein in ways that could allow it to kill neurons, causing dementia.

The bacteria and its enzymes were found at higher levels in those who had experienced worse cognitive decline, and had more amyloid and tau accumulations. The team also found the bacteria in the spinal fluid of living people with Alzheimer’s, suggesting that this technique may provide a long-sought after method of diagnosing the disease.

When the team gave P. gingivalis gum disease to mice, it led to brain infection, amyloid production, tangles of tau protein, and neural damage in the regions and nerves normally affected by Alzheimer’s.

Cortexyme had previously developed molecules that block gingipains. Giving some of these to mice reduced their infections, halted amyloid production, lowered brain inflammation and even rescued damaged neurons.

The team found that an antibiotic that killed P. gingivalis did this too, but less effectively, and the bacteria rapidly developed resistance. They did not resist the gingipain blockers. “This provides hope of treating or preventing Alzheimer’s disease one day,” says Singhrao.

New treatment hope

Some brain samples from people without Alzheimer’s also had P. gingivalis and protein accumulations, but at lower levels. We already know that amyloid and tau can accumulate in the brain for 10 to 20 years before Alzheimer’s symptoms begin. This, say the researchers, shows P. gingivalis could be a cause of Alzheimer’s, but it is not a result.

Gum disease is far more common than Alzheimer’s. But “Alzheimer’s strikes people who accumulate gingipains and damage in the brain fast enough to develop symptoms during their lifetimes,” says Lynch. “We believe this is a universal hypothesis of pathogenesis.”

Cortexyme reported in October that the best of their gingipain blockers had passed initial safety tests in people, and entered the brain. It also seemed to improve participants with Alzheimer’s. Later this year the firm will launch a larger trial of the drug, looking for P. gingivalis in spinal fluid, and cognitive improvements, before and after.

They also plan to test it against gum disease itself. Efforts to fight that have led a team in Melbourne to develop a vaccine for P. gingivalis that started tests in 2018. A vaccine for gum disease would be welcome – but if it also stops Alzheimer’s the impact could be enormous.

Journal reference: Science Advances

https://www.newscientist.com/article/2191814-we-may-finally-know-what-causes-alzheimers-and-how-to-stop-it/


Coloured positron emission tomography (PET, centre) and computed tomography (CT, left) scans of the brain of a 62-year-old woman with Alzheimer’s disease.

By Pam Belluck

In dementia research, so many paths have led nowhere that any glimmer of optimism is noteworthy.

So some experts are heralding the results of a large new study, which found that people with hypertension who received intensive treatment to lower their blood pressure were less likely than those receiving standard blood pressure treatment to develop minor memory and thinking problems that often progress to dementia.

The study, published Monday in JAMA, is the first large, randomized clinical trial to find something that can help many older people reduce their risk of mild cognitive impairment — an early stage of faltering function and memory that is a frequent precursor to Alzheimer’s disease and other dementias.

The results apply only to those age 50 or older who have elevated blood pressure and who do not have diabetes or a history of stroke. But that’s a condition affecting a lot of people — more than 75 percent of people over 65 have hypertension, the study said. So millions might eventually benefit by reducing not only their risk of heart problems but of cognitive decline, too.

“It’s kind of remarkable that they found something,” said Dr. Kristine Yaffe, a professor of psychiatry and neurology at University of California San Francisco, who was not involved in the research. “I think it actually is very exciting because it tells us that by improving vascular health in a comprehensive way, we could actually have an effect on brain health.”

The research was part of a large cardiovascular study called Sprint, begun in 2010 and involving more than 9,000 racially and ethnically diverse people at 102 sites in the United States. The participants had hypertension, defined as a systolic blood pressure (the top number) from 130 to 180, without diabetes or a history of stroke.

These were people who could care for themselves, were able to walk and get themselves to doctors’ appointments, said the principal investigator, Dr. Jeff D. Williamson, chief of geriatric medicine and gerontology at Wake Forest School of Medicine.

The primary goal of the Sprint study was to see if people treated intensively enough that their blood pressure dropped below 120 would do better than people receiving standard treatment which brought their blood pressure just under 140. They did — so much so that in 2015, the trial was stopped because the intensively treated participants had significantly lower risk of cardiovascular events and death that it would have been unethical not to inform the standard group of the benefit of further lowering their blood pressure.

But the cognitive arm of the study, called Sprint Mind, continued to follow the participants for three more years even though they were no longer monitored for whether they continued with intensive blood pressure treatment. About 8,500 participants received at least one cognitive assessment.

The primary outcome researchers measured was whether patients developed “probable dementia.” Fewer patients did so in the group whose blood pressure was lowered to 120. But the difference — 149 people in the intensive-treatment group versus 176 people in the standard-treatment group — was not enough to be statistically significant.

But in the secondary outcome — developing mild cognitive impairment or MCI — results did show a statistically significant difference. In the intensive group, 287 people developed it, compared to 353 people in the standard group, giving the intensive treatment group a 19 percent lower risk of mild cognitive impairment, Dr. Williamson said.

Because dementia often develops over many years, Dr. Williamson said he believes that following the patients for longer would yield enough cases to definitively show whether intensive blood pressure treatment helps prevent dementia too. To find out, the Alzheimer’s Association said Monday it would fund two more years of the study.

“Sprint Mind 2.0 and the work leading up to it offers genuine, concrete hope,” Maria C. Carrillo, the association’s chief science officer, said in a statement. “MCI is a known risk factor for dementia, and everyone who experiences dementia passes through MCI. When you prevent new cases of MCI, you are preventing new cases of dementia.”

Dr. Yaffe said the study had several limitations and left many questions unanswered. It’s unclear how it applies to people with diabetes or other conditions that often accompany high blood pressure. And she said she would like to see data on the participants older than 80, since some studies have suggested that in people that age, hypertension might protect against dementia.

The researchers did not specify which type of medication people took, although Dr. Williamson said they plan to analyze by type to see if any of the drugs produced a stronger cognitive benefit. Side effects of the intensive treatment stopped being monitored after the main trial ended, but Dr. Williamson said the biggest negative effect was dehydration.

Dr. Williamson said the trial has changed how he treats patients, offering those with blood pressure over 130 the intensive treatment. “I’ll tell them it will give you a 19 percent lower chance of developing early memory loss,” he said.

Dr. Yaffe is more cautious about changing her approach. “I don’t think we’re ready to roll it out,” she said. “It’s not like I’m going to see a patient and say ‘Oh my gosh your blood pressure is 140; we need to go to 120.’ We really need to understand much more about how this might differ by your age, by the side effects, by maybe what else you have.”

Still, she said, “I do think the take-home message is that blood pressure and other measures of vascular health have a role in cognitive health,” she said. “And nothing else has worked.”

Levels of a protein called neurofilament light chain increase in the blood and spinal fluid of some Alzheimer’s patients 16 years before they develop symptoms, according to a study published January 21 in Nature Medicine.

The results suggest that neurofilament light chain (NfL), which is part of the cytoskeleton of neurons and has previously been tied to brain damage in mice, could serve as a biomarker to noninvasively track the progression of the disease. “This is something that would be easy to incorporate into a screening test in a neurology clinic,” coauthor Brian Gordon, an assistant professor of radiology at Washington University, says in a press release.

Gordon and his colleagues measured NfL in nearly 250 people carrying an Alzheimer’s-risk allele and more than 160 of their relatives who did not carry the variant. They found that those at risk of developing the disease had higher levels of the protein early on, and that NfL levels in both the blood and spinal fluid were on the rise well before the patients began to show signs of neurodegeneration, more than 16 years before disease onset.

Examining a subset of the patients more closely, the team saw that the rate of increase in NfL correlated with the shrinkage of a brain region called the precuneus, and patients whose NfL levels were rising rapidly tested worse on cognitive tests. “It is not necessarily the absolute levels which tell you your neurodegeneration is ongoing, it is the rate of change,” coauthor Mathias Jucker, a professor of cellular neurology at the German Center for Neurodegenerative Diseases in Tübingen, tells The Guardian.

The Alzheimer’s-linked mutation carried by patients examined in this study only affects about 1 percent of people who get the neurodegenerative disease, so the approach must be validated in a broader patient population, James Pickett, the head of research at the Alzheimer’s Society, tells The Guardian.

“We validated it in people with Alzheimer’s disease because we know their brains undergo lots of neurodegeneration, but this marker isn’t specific for Alzheimer’s,” Gordon says in the release. “I could see this being used in the clinic in a few years to identify signs of brain damage in individual patients.”

Meanwhile, a research team at Seoul National University in South Korea described another potential blood test for Alzheimer’s, focusing on the tau and amyloid proteins known to be associated with the disease. According to their study published today in Brain, blood levels of tau and amyloid correlate with how much tau has accumulated in the brain, as well as other markers of neurodegeneration such as hippocampal volume. “These results indicate that combination of plasma tau and amyloid-β1–42 levels might be potential biomarkers for predicting brain tau pathology and neurodegeneration,” the researchers write in their report.

https://www.the-scientist.com/news-opinion/protein-changes-detected-in-blood-years-before-alzheimers-onset-65347


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.