All articles tagged with #myelin
A study suggests a yak-adapted gene called Restat, which boosts a vitamin A–related molecule (ATDR), may help repair the myelin sheath around nerves. In mice engineered with the mutation and exposed to low-oxygen conditions, researchers saw thicker, healthier myelin and faster repair after damage, offering a potential new avenue for treating multiple sclerosis and possibly other nerve-damage conditions.
A multinational study introduces Xi–αNET, a generative model that links EEG signals (the background ξ and alpha rhythms) to the brain’s physical wiring and axonal conduction delays across ages 5–100 using the HarMNqEEG dataset. The findings show alpha frequency scales with myelin-driven conduction speed, producing a U-shaped trajectory of conduction delays with age and slower rhythms in older adults; the model also detects Parkinson’s-related alpha slowing, highlighting potential EEG-based brain-health benchmarks and early disease flagging via normative charts.
A gain-of-function mutation in the high-altitude Retsat gene helps restore myelin and promote nerve repair in mice by boosting vitamin A–derived metabolites that support oligodendrocyte maturation. The study, published in Neuron (March 13, 2026), suggests a natural, body-made pathway to treat myelin-related conditions such as multiple sclerosis and cerebral palsy, potentially reducing the need for immune-targeting drugs by enhancing innate regenerative processes.
University of Connecticut researchers report that the anti-aging drug combination dasatinib and quercetin (D+Q) causes significant myelin loss and corpus callosum damage in mice, with younger animals affected more. The oligodendrocytes shift to a less mature, energy-stressed state, suggesting safety concerns for preventive use and offering new clues for understanding multiple sclerosis.
A study links a Tibetan high-altitude gene mutation (Retsat) found in yaks to improved myelin protection and rapid repair in a mouse model, via elevated ATDR (a vitamin A metabolite) that promotes oligodendrocyte maturation, pointing to potential MS therapies using existing biological pathways.
A rat study shows psilocybin and MDMA trigger adaptive myelination, repairing the brain’s insulation (myelin) in fear circuits and producing long-lasting reductions in anxiety-like behavior; blocking myelin repair abolishes the benefits, indicating myelin remodeling is a key mechanism for durable psychedelic-assisted PTSD therapy and should complement, not replace, psychotherapy.
New research links sleep loss to damage in oligodendrocytes that insulate neurons, thinning myelin and slowing brain signaling in rats, while human MRI data show reduced white-matter integrity with poorer sleep. In rats, sleep deprivation disrupted cholesterol handling by oligodendrocytes and slowed inter-regional communications, but restoring cholesterol transfer with cyclodextrin improved function, suggesting a potential target for mitigating sleep-loss effects, though human confirmation is needed.
Scientists discovered that losing a small, critical segment of myelin disrupts brain communication by impairing the transmission of signals between the cortex and thalamus, which can lead to cognitive issues similar to those seen in Multiple Sclerosis. The study highlights the importance of myelin in maintaining the structure of neural information transfer and suggests potential avenues for future recovery strategies.
A five-year study supported by NSF investigates how dopamine may regulate myelin plasticity in the brain, particularly in response to social isolation, with implications for understanding and treating neuropsychiatric and neurodegenerative conditions.
A study published in Nature Metabolism found that running a marathon causes temporary reductions in brain myelin levels, which recover within weeks, suggesting that marathon running is not harmful to brain health but may instead reflect metabolic adaptation and flexibility.
A mouse study suggests that herpes simplex virus type 1 (HSV-1) may contribute to multiple sclerosis (MS) by damaging myelin, with findings indicating that blocking the MLKL protein can prevent myelin loss and neurological damage, highlighting potential new treatment avenues.
A cell study shows that pro-inflammatory molecules like TNF-alpha and interferon gamma impair the growth of myelin-producing cells in the brain, potentially contributing to multiple sclerosis by hindering myelin repair. The research suggests that promoting oligodendrocyte development while preventing astrocyte-like transformation could be a promising therapeutic strategy for MS.
Researchers at Tel Aviv University have discovered that SHANK3 gene mutations, linked to autism, impair not only neurons but also oligodendrocytes, which are crucial for myelin production. This disruption reduces brain signal efficiency. Using gene therapy, they successfully repaired these cells in mice and human-derived stem cells, restoring their function and myelin production. This study highlights the significant role of oligodendrocytes in autism and suggests potential new treatments targeting myelin dysfunction.
Researchers have discovered that an RNA derived from a domesticated virus, RNLTR12-int, plays a crucial role in regulating the gene that encodes myelin, a key nerve protein. By inhibiting RNLTR12-int, the production of myelin was significantly reduced in rats, zebrafish, and frogs, leading to simpler structures in the cells that produce myelin. This finding sheds light on the evolutionary history of myelin and its impact on the development and function of vertebrate brains.
Dr. Mary Bartlett Bunge, a pioneering figure in neuroscience, passed away at the age of 92. Alongside her husband, she conducted groundbreaking research on spinal cord injuries, ultimately discovering a promising treatment for paralyzed patients. Her focus on myelin, the protective coating around nerve fibers, led to new ways to promote nervous system regeneration, offering hope to countless individuals worldwide.