A team of neurologists, neuroradiologists and biomaterials specialists affiliated with several institutions in Spain has found that marathon runners undergo a reversible reduction in myelin in the brain during a race. In their study published in the journal Nature Metabolism, the group analyzed MRI scans of marathon runners before and after a race and then at later intervals to learn more about how participating in long races impacts the brain.

The editors at the journal have published a Research Briefing that outlines the work in the same issue and suggest that the team’s findings could influence the understanding of brain metabolism.

The researchers recruited 10 runners—eight male and two female—and performed MRI scans of their brains before they ran a 42K marathon. They administered a second scan 24 to 48 hours later. Two of the runners received an MRI two weeks later, and six runners were scanned two months after the race as a follow-up.

Research conducted by the National Institute on Drug Abuse, the Substance Abuse and Mental Health Services Administration, and the Centers for Disease Control and Prevention reveals that 1 in 4 adults using prescription stimulants engaged in misuse, and nearly 1 in 10 met the criteria for prescription stimulant use disorder (PSUD).

Findings show that amphetamine users were more likely to experience PSUD than those prescribed methylphenidate. Increased prescribing rates, particularly among middle-aged women, were observed, yet this demographic exhibited lower misuse rates than younger adults.

Concerns over stimulant misuse have grown as prescribing rates for these medications, commonly used to treat attention-deficit/hyperactivity disorder (ADHD), have increased. Clinical practice guidelines for adult ADHD remain absent, leading to variations in diagnosis and treatment. Questions about appropriate use persist as research indicates both the protective benefits of ADHD pharmacotherapy and its potential risks, including misuse, overprescription, and development of use disorders.

Sleep isn’t just a luxury, it’s a vital process that helps our bodies repair and rejuvenate. Researchers have started to uncover how the quality and timing of sleep can affect more than just how rested we feel—it might also affect the very blueprint of our cells: our DNA.

A new study from Canada found that melatonin, a hormone known for its role in regulating sleep, might help reverse some of the DNA damage caused by years of poor sleep.

Melatonin is produced by the pineal gland in our brains when darkness falls. It signals to our bodies that it’s time to wind down and prepare for sleep. Beyond its sleep-inducing properties, melatonin is also a powerful antioxidant.

Dr. Michael Levin is on the verge of revolutionizing medicine by unlocking the bioelectric code that governs how cells communicate, heal, and build complex structures. His work reveals that intelligence exists at every level of biology—allowing us to reprogram tissues, regenerate limbs, and even suppress cancer by restoring cellular memory and connection.

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Ubiquitin marks proteins for degradation, whereby ubiquitin molecules can be combined in different types and numbers forming different chains. Researchers at the Max Planck Institute of Biochemistry (MPIB) have developed the new UbiREAD technology to decode the various combinations of ubiquitin molecules—the ubiquitin code—which determine how proteins are degraded in cells.

Using UbiREAD, scientists label fluorescent proteins with specific ubiquitin codes and track their degradation in cells. The study, published in Molecular Cell, revealed which ubiquitin code can or cannot induce intracellular protein degradation.

Proteins are the building blocks of life, maintaining cellular structure and function. However, when proteins become damaged, misfolded, or obsolete, they can lead to a range of diseases, from Alzheimer’s and Parkinson’s to cancer and muscular dystrophy. To prevent this, cells have developed a sophisticated system to mark unwanted proteins for degradation with a small protein called ubiquitin.

Type 2 diabetes may quietly alter the brain in ways that mimic early Alzheimer’s, weakening reward perception and memory signals in a key brain area called the anterior cingulate cortex (ACC). In a rat study, diabetic animals still behaved normally but processed rewarding locations differently, s

The study is the first to use a cutting-edge technique called spatial transcriptomics on human clinical-trial brains with Alzheimer’s disease. The technique allows scientists to pinpoint the specific spatial location of gene activity inside a tissue sample.

By analyzing donated brain tissue from deceased people with Alzheimer’s disease who received amyloid-beta immunization and comparing it to those who did not, the scientists found that when these treatments work, the brain’s immune cells (called microglia) don’t just clear plaques — they also help restore a healthier brain environment.

But not all microglia are created equal. Some are quite effective at removing plaques, while others struggle, the study found. Also, microglia in treated brains adopt distinct states depending on the brain region and type of immunization. Lastly, certain genes, like TREM2 and APOE, are more active in microglia in response to treatment, helping these cells remove amyloid beta plaques, according to the findings.

“The idea is that in people who already have Alzheimer’s disease, yes, you can maybe remove amyloid, but if the tau spread has been set in motion, you are fighting an uphill battle,” the author said. “But maybe, if you treat people so early that they don’t yet have tau pathology, you can stop the domino effect from happening. Our study is the first to identify the mechanisms in microglia, the brain’s immune cells, that help limit the spread of amyloid in certain brain regions following treatment with amyloid-targeting drugs.

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For more than three decades, scientists have been racing to stop Alzheimer’s disease by removing amyloid beta plaques — sticky clumps of toxic protein that accumulate in the brain. Now, a new study suggests a promising alternative: enhancing the brain’s own immune cells to clear these plaques more effectively.

The findings could reshape the future of Alzheimer’s treatments, shifting the focus from simply removing plaques to harnessing the brain’s natural defenses.

Earlier attempts at an Alzheimer’s vaccine failed when the immune system’s response caused dangerous brain swelling. Even today’s FDA-approved antibody treatments remain controversial, offering only modest benefits with potential side effects and high-price points.