A finger prick blood test combined with online brain testing—all done from home—could one day effectively identify people’s risk of developing dementia, according to a new study.

Led by the University of Exeter and published in Nature Communications, the study found that the level of proteins linked to dementia which were measured in the postal blood test were linked to performance on a series of brain tests. The research paper is titled “Alzheimer’s Disease blood biomarkers measured through remote capillary sampling correlate with cognition in older adults.”

The research concludes that at-home testing could be a way to identify people at highest risk of dementia, who could then be prioritized for further testing, treatment and support. It could also identify people at low risk who could be given assurance, as well as those with moderate risk who may benefit from monitoring and guidance on reducing their risk in future.

Professor Anne Corbett, of the University of Exeter Medical School, led the research, and said, “Our previous research has shown that a finger-prick blood test can effectively be taken at home and posted to labs, and that we can identify the biomarkers in blood linked to dementia. This new study builds on that to show that we can link these biomarkers with performance on brain tests, giving us a potential way to predict the risk of dementia.

“This work raises the potential for screening people for their risk without the need for clinic visits or complex clinical assessments. It would ensure the people at highest risk could be prioritized for monitoring and diagnosis, unlocking the best support and treatment for those that need it most.”

The research was conducted in the online PROTECT study, in which more than 30,000 UK participants aged over 40 took regular cognitive tests to measure memory, attention and executive function, or decision-making skills.

The research included 174 PROTECT participants who were sent the at-home tests and administered it themselves, posting it back to the team. The researchers measured two proteins—Ptau 217, which is linked to Alzheimer’s disease, and Gfap, linked to broader brain decline.

They found that performance on the brain tests correlated with the presence of the proteins, with tau emerging with the strongest links. This enabled the team to categorize people at low, medium and high risk.

Professor Clive Ballard, of the University of Exeter Medical School, was involved in the research. He said, “Almost a million people in the UK are estimated to have dementia, yet at the moment, only one in a thousand people with the earliest signs of brain decline receives a specialist evaluation.

“Our approach of combining our robust cognitive testing with measuring proteins via a postal blood test could provide a straightforward, efficient and cost-effective method to reach large numbers of people in the community who would not otherwise be prioritized for the next steps of diagnosis or support and to optimize the clinical pathway to enable early detection of those at highest risk.

“We need further research to validate this approach, and I’d encourage anyone aged 40 or over to join us by signing up to PROTECT.”

Professor Marian Knight, NIHR Scientific Director for NIHR Infrastructure, said, “The potential of this combination of cognitive and blood tests—both of which can be done at home—is really exciting.

“Not only could it reduce the burden on the NHS by screening people in their own homes rather than in hospitals or clinics, but it might also mean we can identify people with dementia earlier, tailor treatments more effectively, and improve outcomes for patients.

“This is a fantastic example of research teams in NIHR infrastructure working together to deliver real change for the public and the NHS, in line with government priorities.”

Researchers at UC San Francisco and Imperial College London have shown that a single dose of psilocybin, the psychedelic compound found in magic mushrooms, causes likely anatomical brain changes that last for up to a month after the experience.

The study, published in Nature Communications, was done in healthy volunteers who had never taken a psychedelic, but it may help explain psilocybin’s therapeutic effects on conditions like depression, anxiety, and addiction. The researchers link temporary shifts in brain “entropy”—which is the diversity of neural activity occurring in the brain—to insight. This suggests the psychedelic trip itself is important to the drug’s longer-term therapeutic effects.

The researchers found that a high dose of psilocybin led to increased entropy in the minutes and hours after taking the drug. The degree of entropy predicted how much insight, or emotional self-awareness, the participants felt the next day; and this, in turn, forecasted improvements in their sense of well-being a month later.

“Psychedelic means ‘psyche-revealing,’ or making the psyche visible,” said senior author Robin Carhart-Harris, Ph.D., the Ralph Metzner Distinguished Professor of Neurology at UCSF.

“Our data shows that such experiences of psychological insight relate to an entropic quality of brain activity and how both are involved in causing subsequent improvements in mental health. It suggests that the trip—and its correlates in the brain—is a key component of how psychedelic therapy works.”

A careful assessment of psilocybin’s effects

Researchers used an assortment of brain imaging and brain measurement techniques, some of which were done during the peak of the psychedelic experience, as well as before and one-month after.

None of the 28 people in the study had a diagnosed mental health condition, which gave the scientists greater freedom to do more testing.

In the first part of the experiment, the subjects were given a 1 mg dose of psilocybin, which the researchers regarded as a placebo, and then monitored with electroencephalography (EEG), which records brain activity from electrodes on the scalp.

Over the next few weeks, the researchers measured their subjects’ psychological insight, well-being and cognitive ability. They examined brain activity with functional MRI (fMRI) and brain connectivity with diffusion tensor imaging (DTI).

One month after the placebo, the subjects were given 25 mg of psilocybin, a dose capable of eliciting a strong psychedelic trip. During the experience, researchers again measured the subjects’ brain activity with EEG, and in the following weeks they repeated the same tests they had given after the 1 mg dose.

This enabled the scientists to compare the effects of the psychedelic trip on the brain and mind to the effects of the placebo.

Greater ‘information’ in the brain after psilocybin

Within 60 minutes of taking the 25 mg dose of psilocybin, EEG revealed higher entropy, suggesting that the brain was processing a richer body of information under the psychedelic.

A month later, the researchers looked at their subjects’ brains with DTI, which measures the diffusion of water along neural tracts in the brain, and found that they were denser and had more integrity. This is the opposite of what happens in aging, which makes these tracts more diffuse.

The researchers cautioned that more work needs to be done to better understand the meaning of this change, but the result is a never-before-seen sign of how psychedelics can change the brain.

Enduring improvements in well-being

The day after the 25 mg dose, all but one of the 28 subjects rated the trip as the “single most” unusual state of consciousness they had ever experienced. The remaining person rated it as among the top five.

The people in the study also said they had experienced more psychological insight after taking the 25 mg of psilocybin than they had after the 1 mg placebo.

The subjects reported increased well-being two and four weeks after the study. This was measured from responses to statements like, “I’ve been feeling optimistic about the future” and “I’ve been dealing with problems well.” A month after the study, they also did better on a test of cognitive flexibility.

“Psilocybin seems to loosen up stereotyped patterns of brain activity and give people the ability to revise entrenched patterns of thought,” said Taylor Lyons, Ph.D., a research associate at Imperial College London and the first author of the paper. “The fact that these changes track with insight and improved well-being is especially exciting.”

A freer brain and a healthier mind?

The scientists found that the subjects who had experienced the largest increases in brain entropy in the minutes to hours after taking psilocybin were the most likely to have increased insight the next day and increased well-being a month later. They conclude that improved well-being was driven by the experience of insight.

The findings could improve treatment for people with mental illness with psilocybin, for example, by ensuring that the right dosage is used to produce the right amount of brain entropy to promote insight.

“We already knew psilocybin could be helpful for treating mental illness,” Carhart-Harris said. “But now we have a much better understanding of how.”

Omega-3 supplements are popular among many older adults to help combat age-related issues. They are often marketed as supporting cardiovascular health and reducing the risk of cognitive decline and dementia. However, a new study published in The Journal of Prevention of Alzheimer’s Disease suggests that these oral capsules may actually be linked to a faster decline in cognitive function.

Many senior citizens swear by oral supplements and the benefits they bring. However, the scientific evidence is mixed. While animal and observational studies have indicated possible protective effects on the aging brain, controlled trials with humans have not shown such cognitive benefits.

To try to find definitive answers about whether the supplements actually slow cognitive decline, researchers from China used long-term patient data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) and studied highly detailed brain scans.

The omega-3 paradox

The study examined cognitive and brain imaging changes over five years in 273 omega-3 users and compared them with a control group of 546 non-users. These were matched for age, sex, genetics, and diagnosis.

The results revealed that participants taking omega-3 supplements showed a more rapid decline across the three primary cognitive assessments (MMSE, ADAS-Cog13, and CDR-SB) each person completed during the study.

This pattern remained the same regardless of genetics. Both groups had the same number of people with the APOE ε4 gene, which is associated with increased risk for Alzheimer’s. This suggests the difference in decline was unlikely to be explained by this major genetic risk factor alone.

To see why this might be the case, the researchers studied brain scans to look for physical changes. The faster decline did not appear to be caused by the typical signs of Alzheimer’s, such as the buildup of amyloid plaques or abnormal clumps of tau proteins.

Glucose and the aging brain

Instead, the scans revealed a significant drop in brain glucose metabolism, which the research team believes may be linked to omega-3 supplementation. This reduction is often associated with synaptic dysfunction, meaning that while the physical structure of the brain may remain relatively intact, communication between brain cells may be less efficient.

“Omega-3 supplementation may be associated with accelerated cognitive decline in older adults, potentially through adverse effects on cerebral synaptic function rather than classical AD proteinopathies,” wrote the study authors in their paper.

The team points out that their results are not conclusive. This was an observational study, not a clinical trial, that identified an association rather than a definitive cause. Nonetheless, it’s a correlation that needs further investigation.

“These findings challenge the prevailing view of omega-3 as uniformly beneficial and highlight the need for a cautious reassessment of its widespread use for cognitive protection.”

Multiple sclerosis (MS) is most prevalent in Northern Europe and Canada, and more common in the northernmost latitudes. In recent years, the number of cases has grown, particularly among women. The disease causes the patient’s own immune system to attack a protective coating known as myelin that surrounds nerve cells. When this sheath is destroyed, neuronal function decreases and the cells can ultimately die. This can result in visual disturbances, fatigue, mobility difficulties, and other neurological symptoms that may be permanent.

No treatment for neural damage

Current MS drugs suppress the immune system’s overactivation but are unable to repair the neural damage caused. This is a particular problem in the progressive form of the disease, where damage accumulates slowly over the years.

Researchers have long sought ways to initiate remyelination, a process where the destroyed myelin sheath grows back and the neurons recover. However, all drug candidates trialed so far have failed. The problem is that, particularly in the later stages of MS, the disease creates in the central nervous system local tissue conditions that inhibit remyelination.

Two solutions with the same outcome

In his doctoral thesis, Tapani Koppinen from Associate Professor Merja Voutilainen’s research group identified two different approaches for enhancing remyelination.

In the first approach, a drug molecule targets a stress mechanism intrinsic to brain cells. In areas damaged by MS, this stress response is constantly in overdrive, effectively preventing tissue-repairing cells from doing their job. When the mechanism was blocked using the new drug molecule, remyelination was significantly enhanced and accelerated in brain tissue with MS-like damage. The study was published in the Molecular Therapy journal in February.

The second approach focuses on scar tissue formed around affected areas, which serves as a physical barrier to neural regeneration. By affecting the composition of this scar tissue with the second drug molecule, this approach also succeeded in promoting neuronal recovery. An article focusing on this approach was published in November in the journal Neuropharmacology.

Surprisingly, these two drugs based on entirely different mechanisms led to very similar results: significant remyelination and reduced neuroinflammation in disease models, that is, animal and cell tests modeling the tissue pathology of MS.

First drug that boosts remyelination requires further research

For the time being, the results were achieved in laboratory animals and cell models. The more complex tissue conditions of human MS make it necessary to investigate the efficacy of the drug molecules in humans. One challenge for drugs targeting the brain is the blood-brain barrier, which blocks many substances from entering the brain. The researchers nevertheless demonstrated that both molecules effectively reach the central nervous system in laboratory animals.

“The goal is to enable the molecules we have developed to reach clinical trials, which could one day produce the first drugs that enhance remyelination in MS. In the meantime, our findings can help in investigating the pathogenic mechanisms of MS that inhibit remyelination,” Koppinen says.