Posts Tagged ‘brain’

Scientists have peered inside the brain to show how taking DMT affects human consciousness by significantly altering the brain’s electrical activity.

DMT (or dimethyltryptamine) is one of the main psychoactive constituents in ayahuasca, the psychedelic brew traditionally made from vines and leaves of the Amazon rainforest. The drink is typically prepared as part of a shamanic ceremony and associated with unusual and vivid visions or hallucinations.

The latest study is the first to show how the potent psychedelic changes our waking brain waves – with researchers comparing its powerful effects to ‘dreaming while awake’.

The work, led by researchers from the Centre for Psychedelic Research at Imperial College London and published today in the journal Scientific Reports, may help to explain why people taking DMT and ayahuasca experience intense visual imagery and immersive ‘waking-dream’ like experiences.

DMT is a naturally occurring chemical found in miniscule amounts in the human brain but also in larger amounts in a number of plant species around the world.

Accounts from people who have taken DMT report intense visual hallucinations often accompanied by strong emotional experiences and even ‘breakthroughs’ into what users describe as an alternate reality or dimension.

But scientists are interested in using the powerful psychoactive compound for research as it produces relatively short but intense psychedelic experiences, providing a window for collecting data on brain activity when consciousness is profoundly altered.

In the latest study, the Imperial team captured EEG measures from healthy participants in a clinical setting, in a placebo-controlled design.

A total of 13 participants were given an intravenous infusion of DMT at the National Institute for Health Research (NIHR) Imperial Clinical Research Facility.

Volunteers were fitted with caps with electrodes to measure the brain’s electrical activity, before, during and after their infusion, with the peak of the psychedelic experience lasting around 10 minutes.

Analysis revealed that DMT significantly altered electrical activity in the brain, characterised by a marked drop off in alpha waves – the human brain’s dominant electrical rhythm when we are awake. They also found a short-lived increase in brainwaves typically associated with dreaming, namely, theta waves.

In addition to changes in the types of brainwaves, they also found that, overall, brain activity became more chaotic and less predictable – the opposite to what is seen in states of reduced consciousness, such as in deep sleep or under general anaesthesia.

“The changes in brain activity that accompany DMT are slightly different from what we see with other psychedelics, such as psilocybin or LSD, where we see mainly only reductions in brainwaves,” said lead author Christopher Timmermann, from the Centre for Psychedelic Research.

“Here we saw an emergent rhythm that was present during the most intense part of the experience, suggesting an emerging order amidst the otherwise chaotic patterns of brain activity. From the altered brainwaves and participants’ reports, it’s clear these people are completely immersed in their experience – it’s like daydreaming only far more vivid and immersive, it’s like dreaming but with your eyes open.”

Mr Timmermann explains that while it’s unclear as to whether DMT may have any clinical potential at this stage, the group hopes to take the work further by delivering a continuous infusion of DMT to extend the window of the psychedelic experience and collect more data.

The team says future studies could include more sophisticated measurements of brain activity, such as fMRI, to show which regions and networks of the brain are affected by DMT. They believe the visual cortex, the large area towards the back of the brain, is likely to be involved.

Dr Robin Carhart-Harris, head of Centre for Psychedelic Research, said: “DMT is a particularly intriguing psychedelic. The visual vividness and depth of immersion produced by high-doses of the substance seems to be on a scale above what is reported with more widely studied psychedelics such as psilocybin or ‘magic mushrooms’.

“It’s hard to capture and communicate what it is like for people experiencing DMT but likening it to dreaming while awake or a near-death experience is useful.

“Our sense it that research with DMT may yield important insights into the relationship between brain activity and consciousness, and this small study is a first step along that road.”

https://www.eurekalert.org/pub_releases/2019-11/icl-acc111819.php

New research has found that people who are illiterate, meaning they never learned to read or write, may have nearly three times greater risk of developing dementia than people who can read and write. The study is published in the November 13, 2019, online issue of Neurology®, the medical journal of the American Academy of Neurology.

According to the United States Department of Education, approximately 32 million adults in the country are illiterate.

“Being able to read and write allows people to engage in more activities that use the brain, like reading newspapers and helping children and grandchildren with homework,” said study author Jennifer J. Manly, Ph.D., of Columbia University Vagelos College of Physicians and Surgeons in New York. “Previous research has shown such activities may reduce the risk of dementia. Our new study provides more evidence that reading and writing may be important factors in helping maintain a healthy brain.”

The study looked at people with low levels of education who lived in northern Manhattan. Many were born and raised in rural areas in the Dominican Republic where access to education was limited. The study involved 983 people with an average age of 77. Each person went to school for four years or less. Researchers asked each person, “Did you ever learn to read or write?” Researchers then divided people into two groups; 237 people were illiterate and 746 people were literate.

Participants had medical exams and took memory and thinking tests at the beginning of the study and at follow-up appointments that occurred every 18 months to two years. Testing included recalling unrelated words and producing as many words as possible when given a category like fruit or clothing.

Researchers found of the people who were illiterate, 83 of 237 people, or 35 percent, had dementia at the start of the study. Of the people who were literate, 134 of 746 people, or 18 percent, had dementia. After adjusting for age, socioeconomic status and cardiovascular disease, people who could not read and write had nearly a three times greater chance of having dementia at the start of the study.

Among participants without dementia at the start of the study, during follow-up an average of four years later, 114 of 237 people who were illiterate, or 48 percent, had dementia. Of the people who were literate, 201 of 746 people, or 27 percent, had dementia. After adjusting for age, socioeconomic status and cardiovascular disease, researchers found that people who could not read and write were twice as likely to develop dementia during the study.

When researchers evaluated language, speed, spatial, and reasoning skills, they found that adults who were illiterate had lower scores at the start of the study. But their test scores did not decline at a more rapid rate as the study progressed.

“Our study also found that literacy was linked to higher scores on memory and thinking tests overall, not just reading and language scores,” said Manly. “These results suggest that reading may help strengthen the brain in many ways that may help prevent or delay the onset of dementia.”

Manly continued, “Even if they only have a few years of education, people who learn to read and write may have lifelong advantages over people who never learn these skills.”

Manly said future studies should find out if putting more resources into programs that teach people to read and write help reduce the risk of dementia.

A limitation of the study was that researchers did not ask how or when literate study participants learned to read and write.

The study was supported by the National Institutes of Health and National Institute on Aging.

Story Source:

Materials provided by American Academy of Neurology. Note: Content may be edited for style and length.

Journal Reference:

Miguel Arce Rentería, Jet M.J. Vonk, Gloria Felix, Justina F. Avila, Laura B. Zahodne, Elizabeth Dalchand, Kirsten M. Frazer, Michelle N. Martinez, Heather L. Shouel, Jennifer J. Manly. Illiteracy, dementia risk, and cognitive trajectories among older adults with low education. Neurology, 2019; 10.1212/WNL.0000000000008587 DOI: 10.1212/WNL.0000000000008587

https://www.sciencedaily.com/releases/2019/11/191114180033.htm

By Kristin Houser

Down syndrome is a cognitive disability that can affect a person’s memory or ability to learn — intellectual impairments researchers traditionally thought were untreatable and irreversible.

But now, researchers from the University of California San Francisco and Baylor College of Medicine say they’ve reversed the impairments in mouse models of Down syndrome — potentially foreshadowing an ethically-fraught future in which doctors can do the same for humans with the condition.

All people with Down syndrome share one thing in common: an extra copy of chromosome 21. For that reason, much of the research on Down syndrome has focused on genetics.

But for this new study, published Friday in the prestigious journal Science, researchers focused on the protein-producing cells in the brains of mice with Down syndrome. That led them to the discovery that the animals’ hippocampus regions produced 39 percent less protein than those of typical mice.

Further study led the researchers to conclude that the presence of an extra chromosome likely prompted the animals’ hippocampal cells to trigger the integrated stress response (ISR), which decreased protein production.

“The cell is constantly monitoring its own health,” researcher Peter Walter said in a press release. “When something goes wrong, the cell responds by making less protein, which is usually a sound response to cellular stress. But you need protein synthesis for higher cognitive functions, so when protein synthesis is reduced, you get a pathology of memory formation.”

By blocking the activity of PKR, the enzyme that prompted the ISR in the mouse model’s hippocampal cells, the researchers found they could not only reverse the decreased protein production but also improve the animals’ cognitive function.

Of course, just because something works in mice doesn’t mean it’ll work in humans.

However, when the researchers analyzed postmortem brain tissue samples of people with Down syndrome, they found evidence that the ISR had been activated. They also obtained a tissue sample from a person with Down syndrome who only had the extra copy of chromosome 21 in some of their cells — and those cells were the only ones with ISR activated.

“We started with a situation that looked hopeless,” Walter said. “Nobody thought anything could be done. But we may have struck gold.”

https://futurism.com/neoscope/scientists-reverse-cognitive-deficiets-of-down-syndrome-mice

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

by NICOLETTA LANESE

Kent Kiehl and his research team regularly park their long, white trailer just outside the doors of maximum-security prisons across the US. Inside the vehicle sits the bulky body of a mobile MRI machine. During each visit, people from the prison make their way to and from the vehicle in hourly shifts to have their brains scanned and help to answer an age-old question: What makes a murderer?

“It’s not an uncommon thing for [incarcerated people], while they’re getting a scan, to be like, ‘I’ve always been different. Can you tell me why I’ve always been so different?’” says Kiehl, a neuroscientist at the University of New Mexico and the Albuquerque-based nonprofit Mind Research Network (MRN) who helped design the mobile MRI system back in the early 2000s.


SCAN-MOBILE: Kiehl and his colleagues made more than 75 modifications to a trailer and the MRI system inside to outfit both for the team’s unique research.

The author of The Psychopath Whisperer: The Science of Those Without a Conscience, Kiehl has been fascinated by the criminal mind since he was an undergraduate at the University of California, Davis. Now, as director of mobile imaging at MRN, he oversees efforts to gather brain scans from thousands of people held in US prisons to learn what features, if any, might differ from scans of the general population.

This massive dataset recently allowed Kiehl to examine the brain structures of more than 800 men held in state prisons in New Mexico and Wisconsin in an attempt to distinguish incarcerated people who have committed homicide from those who have committed other crimes.

First, Kiehl and his colleagues laboriously sorted the pool of people who had volunteered for the study into three categories based on their crimes: homicide, violent offenses that were not homicide, or non-violent or minimally violent transgressions. The team relied on official convictions, self-reported homicides, and confidential interviews with participants to determine who attempted or committed murder—both offenses that got a “homicide” label in their dataset.

People charged with felony murder—meaning that they had committed a serious felony that was in some way connected to a person’s death, even though they hadn’t intended to kill the victim—and people whose cases indicated considerable doubt about a judgment of homicide were not counted among murderers. And occasionally, people were moved from another category into the homicide group, Kiehl says. The researchers excluded people with abnormal radiology reports, traumatic brain injury, or diagnosed psychotic disorders from the study.

Controlling for substance use severity, time in prison, age, and IQ, the team analyzed the MRI data to look for differences among the study participants. Compared with the other two groups, the 200 men who had committed homicide showed significantly reduced gray matter in several brain regions that play important roles in behavioral control and social cognition.

“I think that the intriguing thing was, first, that they found a difference,” says Hannes Vogel, a neuropathologist at Stanford University Medical Center who was not involved in the work. “And second of all, that it correlates with some of the brain centers that deal with behavior and social interaction.”

Lora Cope, a neuroscientist who studies substance disorders at the University of Michigan, notes in an email to The Scientist that the team’s mobile MRI system has now been used in correctional facilities all over New Mexico and Wisconsin, and “has really revolutionized this area of research.” Indeed, the MRN has now used the equipment to collect roughly 6,500 scans from more than 3,000 research participants since its first outing in 2007.

Although Cope wasn’t involved in the current project, she worked with Kiehl a few years ago while earning her doctorate at the University of New Mexico. After speaking with members of the Avielle Foundation, named for a six-year-old victim of the 2012 Sandy Hook Elementary School shooting, the two researchers spearheaded a study of more than 150 incarcerated young males, 20 of whom had been convicted of homicide, held at a maximum-security detention facility within the state. “Jeremy, [Avielle’s] father, really wanted to know if there was anything neuroscience could tell us about boys who commit homicide,” says Kiehl.

As in the current study, Cope and Kiehl deployed the mobile scanner to collect MRI scans of the incarcerated teens in New Mexico and discovered differences between those who had committed homicide and their imprisoned peers. The homicide offenders “had significantly less gray matter volume in parts of their temporal lobes,” Cope says. When Kiel compared the data from that study with the results of his latest project, he found a high degree of overlap. “Lo and behold . . . we found and replicated every region that was different in the boys and was different in the adult males, and in the same way,” he says.

The latest study’s finding that MRI data can distinguish homicide offenders not only from people who committed non-violent crimes, but also from those who performed other violent crimes, is particularly interesting, says Harold Koenigsberg, a psychiatrist at Icahn School of Medicine at Mount Sinai. “I would have thought there would be more of an overlap between [homicide and violent non-homicide offenders],” he says. “I’m surprised that it was so specific to homicide.”


ANATOMY OF A MURDERER: Homicide offenders exhibited reduced gray matter density compared with other violent offenders in the regions of the brain highlighted blue and green above.

Koenigsberg notes that homicidal violence can itself be split into two categories: impulsive and instrumental. Impulsive violence is born of unbridled emotions and overblown reactions, a brand of behavior linked to poor frontal lobe functioning and abnormal serotonin levels. Instrumental violence, on the other hand, is premeditated and is associated with other brain changes, such as reduced amygdala activation during emotion processing. “These two groups, we think that they have different biologies,” says Koenigsberg. Kiehl’s dataset could be enriched by adding measures of neurotransmitter release and electrical activity, along with related behavioral assessments, he suggests, and with both functional and structural data, psychologists might learn more about what gives rise to these distinct behavioral phenotypes.

Koenigsberg, Vogel, and Kiehl all note that the structural data collected in the current study cannot on its own be used to predict who has committed homicide, let alone who might in the future. Nonetheless, the paper may find its way into the courtroom, says Vogel. If lawyers felt so inclined, they could try to “find an expert on one side who will quote this [paper]” in defense of someone who has committed a homicide, by arguing a client’s actions were due to brain abnormalities and thus out of his or her control. Or, a prosecutor could potentially use the paper to argue that MRI findings should be admissible as evidence that a defendant has committed a homicide, says Vogel, who has served as a consultant for court cases in California and Nevada, and helped investigate the brain of the Route 91 Harvest music festival shooter in 2017. “But then you’re [also] going to find an expert that will tear that [testimony] to pieces.”

Kiehl notes that his MRI study could also someday contribute to new evidence-based measures of homicidal risk. These measures could supplement current measures of violent behavior, such as psychological questionnaires, if future studies demonstrated they carried predictive weight, he says. Beyond courts of law, he also suggests that understanding how violent behavior arises could pave the way to better psychological treatment aimed at both rehabilitation and prevention.

https://www.the-scientist.com/notebook/secrets-in-the-brains-of-people-who-have-committed-murder-66589


Francisco Lopera, a neurologist at the University of Antioquia in Medellin, Colombia, has been painstakingly collecting brains, birth and death records from one sprawling Colombian family to study Alzheimer’s.Credit…Federico Rios Escobar for The New York Times


A woman with lots of beta-amyloid buildup (red) in her brain remained cognitively healthy for decades.

by Kelly Servick

In 2016, a 73-year-old woman from Medellín, Colombia, flew to Boston so researchers could scan her brain, analyze her blood, and pore over her genome. She carried a genetic mutation that had caused many in her family to develop dementia in middle age. But for decades, she had avoided the disease. The researchers now report that another rare mutation—this one in the well-known Alzheimer’s disease risk gene APOE—may have protected her. They can’t prove this mutation alone staved off disease. But the study draws new attention to the possibility of preventing or treating Alzheimer’s by targeting APOE—an idea some researchers say has spent too long on the sidelines.

“This case is very special,” says Yadong Huang, a neuroscientist at the Gladstone Institutes in San Francisco, California, who was not involved with the research. “This may open up a very promising new avenue in both research and therapy.”

APOE, the strongest genetic risk factor for Alzheimer’s, has three common forms. A variant called APOE2 lowers risk of the disease. The most common variant, APOE3, doesn’t influence risk. APOE4 raises risk; roughly half of the people with the disease have at least one copy of this variant.

Researchers have long contemplated targeting APOE with therapies. A team at Cornell University will soon start a clinical trial that infuses the protective APOE2 gene into the cerebrospinal fluid of people with two copies of APOE4.

But mysteries about APOE have kept it from becoming a front-runner among drug targets. “It does so many things that it’s confusing,” says Eric Reiman, a neuroscientist at the Banner Alzheimer’s Institute in Phoenix and a co-author on the new paper. The APOE protein binds and transports fats and is abundant in the brain. And the APOE4 variant seems to encourage the formation of sticky plaques of the protein beta-amyloid, which clog the brain in Alzheimer’s. But powerful amyloid-busting drugs have repeatedly failed to benefit patients in clinical trials. Some researchers saw no reason to try an APOE-targeting therapy that seemed to be “just a poor man’s antiamyloid treatment,” Reiman says.

The Colombian woman’s case suggests other ways APOE could affect Alzheimer’s risk. The woman participated in a study led by researchers at the University of Antioquia in Medellín that has tracked roughly 6000 members of her extended family. About one-fifth of them carried an Alzheimer’s-causing mutation in a gene called presenilin 1; these carriers generally developed dementia in their late 40s. Yet the woman didn’t show the first signs of the disease until her 70s, even though she, too, carried the mutation. “She’s definitely an outlier,” says cell biologist Joseph Arboleda-Velasquez of Harvard Medical school in Boston. (The research team is keeping the woman’s name confidential to protect her privacy.)

In Boston, a positron emission tomography scan of the woman’s brain revealed more amyloid buildup than in any other family member who has been scanned. “It was very striking,” says Yakeel Quiroz, a clinical neuropsychologist at Massachusetts General Hospital and Harvard Medical School. But the team found no signs of major damage to neurons, and minimal buildup of another Alzheimer’s hallmark: the misfolded protein tau. Whatever protection this woman had didn’t depend on keeping the brain amyloid-free. Instead, her case supports the idea that tau has a “critical role … in the clinical manifestations of Alzheimer’s disease,” says Jennifer Yokoyama, a neurogeneticist at the University of California, San Francisco.

Genome sequencing revealed two copies of a rare mutation in the APOE gene, the researchers report this week in Nature Medicine. First discovered in 1987, the mutation, known as Christchurch, occurs in a region separate from those that determine a person’s APOE2, 3, or 4 status. (The woman has the neutral APOE3 variant.) Previous research found that the Christchurch mutation—like the more common protective APOE2 mutation—impairs APOE’s ability to bind to and clear away fats and sometimes leads to cardiovascular disease.

The researchers also found that the mutation prevents APOE from binding strongly to other molecules called heparan sulfate proteoglycans (HSPGs), which coat neurons and other cells “like a carpet,” says Guojun Bu, a neuroscientist at the Mayo Clinic in Jacksonville, Florida, who has studied the interaction between these molecules and APOE.

APOE2 may also impair the protein’s ability to bind HSPGs. But how that could protect against disease isn’t clear. One possible clue: Research by neuroscientist Marc Diamond of the University of Texas Southwestern Medical Center in Dallas and his colleagues suggest the toxic tau protein relies on HSPGs to help it spread between cells. Maybe the less APOE binds to HSPGs, the harder it is for tau to spread.

But, Diamond cautions, “It will require much more study to understand if this relationship exists.” The Christchurch mutation might have protective effects unrelated to HSPGs; it’s also possible that mutations other than Christchurch protected the woman.

If hampering APOE’s normal binding really staved off her Alzheimer’s, future treatments might aim to mimic that effect. An antibody or small molecule could latch onto the APOE protein to interfere with binding, gene editing could change the structure of APOE to imitate the Christchurch variant, or a “gene silencing” approach could reduce production of APOE altogether.

Reiman hopes the new study will rally researchers to pursue treatments related to APOE. He, Quiroz, Arboleda-Velasquez, and other collaborators also posted a preprint on the medRxiv server on 2 November showing that people with two copies of APOE2 have lower Alzheimer’s risk than previously thought—about 99% lower than people with two copies of APOE4. “When it comes to finding a treatment that could have a profound impact on the disease,” Reiman says, “APOE may be among the lowest hanging fruit.”

https://science.sciencemag.org/content/366/6466/674

By Julie Zaugg and Jared Peng

Authorities in China have approved a drug for the treatment of Alzheimer’s disease, the first new medicine with the potential to treat the cognitive disorder in 17 years.

The seaweed-based drug, called Oligomannate, can be used for the treatment of mild to moderate Alzheimer’s, according to a statement from China’s drug safety agency. The approval is conditional however, meaning that while it can go on sale during additional clinical trials, it will be strictly monitored and could be withdrawn should any safety issues arise.

In September, the team behind the new drug, led by Geng Meiyu at the Shanghai Institute of Materia Medica under the Chinese Academy of Sciences, said they were inspired to look into seaweed due to the relatively low incidence of Alzheimer’s among people who consume it regularly.

In a paper in the journal Cell Research, Geng’s team described how a sugar contained within seaweed suppresses certain bacteria contained in the gut which can cause neural degeneration and inflammation of the brain, leading to Alzheimer’s.

This mechanism was confirmed during a clinical trial carried out by Green Valley, a Shanghai-based pharmaceutical company that will be bringing the new drug to market.

Conducted on 818 patients, the trial found that Oligomannate — which is derived from brown algae — can statistically improve cognitive function among people with Alzheimer’s in as little as four weeks, according to a statement from Green Valley.

“These results advance our understanding of the mechanisms that play a role in Alzheimer’s disease and imply that the gut microbiome is a valid target for the development of therapies,” neurologist Philip Scheltens, who advises Green Valley and heads the Alzheimer Center Amsterdam, said in the statement.

Vincent Mok, who heads the neurology division at the Chinese University of Hong Kong, said the new drug showed “encouraging results” when compared to acetylcholinesterase inhibitors — the existing treatment for mild to severe Alzheimer’s.

“It is just as effective but it has fewer side effects,” he told CNN. “It will also open up new avenues for Alzheimer’s research, focusing on the gut microbiome.”

Since very little is known about the mechanisms of the new drug, Mok said it should also be probed to see if it could have a protective effect and possibly slow down the progression of the disease in patients who have yet to develop strong symptoms of dementia.

The company said Oligomannate will be available in China “very soon,” and it is currently seeking approval to market it abroad, with plans to launch third-phase clinical trials in the US and Europe in early 2020.

Alzheimer’s disease, which starts with memory loss and escalates to severe brain damage, is believed to cause 60% to 70% of the cases of dementia reported worldwide, according to the World Health Organization. Dementia affects an estimated 50 million people worldwide, including 9.5 million people in mainland China, Hong Kong and Taiwan.

Named after Alois Alzheimer, the neuropathologist who discovered the disease in 1906, it has so far confounded researchers and pharmaceutical companies.

In October, US pharmaceutical giant Biogen said it would pursue Food and Drug Administration (FDA) approval for an experimental treatment called aducanumab, after announcing in March it was canceling a large clinical trial for the drug.

Johnson & Johnson, Merck, Pfizer and Eli Lilly have all previously abandoned projects to develop a drug for Alzheimer’s after unsatisfactory clinical data.

https://www.cnn.com/2019/11/03/health/china-alzheimers-drug-intl-hnk-scli/index.html

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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