The study used a weakly supervised deep learning algorithm to analyze human brain autopsy tissues and predict the presence or absence of cognitive impairment. The model identified a signal associated with decreasing myelin staining, which was linked to cognitive impairment in the white matter.
Researchers replaced zebrafish GPR17 receptor gene with human version to study myelin repair in multiple sclerosis. Testing substances in modified fish larvae may lead to quicker and more successful human trials.
The study proposes a model to understand the complications caused by zika virus infection during pregnancy. The researchers found that zika virus alters protein expression in neural cells, affecting energy production and RNA metabolism, which can lead to defective myelination and microcephaly.
A mutation in the TMEM163 zinc transporter gene has been definitively linked to hypomyelinating leukodystrophy, a rare and often fatal neurological disorder. The study's findings provide new insights into the role of zinc in normal brain development, injury, and disease.
Researchers discover that neurons directly contribute to Krabbe disease destruction through enzyme galactosylceramidase. This finding presents a new approach to developing therapies for the rare neurodegenerative disorder.
Researchers found that tenascin C and tenascin R impede the regeneration of myelin sheaths in mice with multiple sclerosis. Mice lacking these proteins rebuilt their myelin sheaths faster and more effectively.
Researchers identified key differences in metabolic processes between brain and spinal cord oligodendrocytes, which could lead to new therapeutic treatments for neurodegenerative diseases. The study also found that targeting a specific cell protein may enhance cholesterol and myelin production.
A new study by University of Bonn researchers found that cow's milk protein casein triggers an autoimmune response in mice, damaging neurons and myelin sheath. This cross-reactivity can occur when the immune system mistakes similar molecules for each other.
Researchers found that myelination, even patchy on interneurons, is required for full inhibitory potential. Myelin loss can cause abnormal brain activity and lead to cognitive impairments.
Research by University of Texas Health Science Center at San Antonio scientists found that mice missing one copy of the Tbx1 gene exhibit slower cognitive processing. The gene's deletion led to diminished myelin insulation around nerves, impacting signal conduction between brain regions.
In chronic damage, new cholesterol production determines the efficiency of repair, with nerve cells contributing to replenishing myelin-forming cells. Treatment with a cholesterol-enriched diet enhances oligodendrocyte progenitor cell proliferation.
A new study suggests that existing drugs for multiple sclerosis may not be effective due to toxic blood leaks in the brain. Researchers have identified a promising alternative treatment option that could improve myelin repair, even in the presence of these harmful elements.
A recent study discovered that brain cells cannot maintain the myelin sheath in the absence of the TDP-43 protein. Restoring cholesterol levels has been proposed as a potential therapeutic strategy for neurodegenerative diseases associated with TDP-43. The research found that oligodendrocytes, responsible for producing myelin, have def...
A new study identifies ten-eleven-translocation 1 (TET1) as a necessary component of myelin repair in adult brains. Higher TET1 levels are needed to form functional myelin in response to injury, which declines with age.
Researchers developed miniature brain models using stem cells from human skin samples to study myelin, an insulating substance that helps nerve cells communicate. The models are a promising platform for studying neurological diseases and testing drugs for conditions linked to myelin loss, including multiple sclerosis.
Researchers have developed a specialized technique to capture unique protein structures associated with neuropathy disorders, such as Charcot Marie Tooth and Dejerine-Sottas syndrome. The technique, ion mobility-mass spectrometry (IM-MS), reveals that an unstable mutant version of the PMP22 protein forms a stable complex called a dimer.
A new study found that myelin loss is a major factor in age-related brain deterioration, leading to cognitive decline and neurodegenerative diseases. The researchers identified a key gene responsible for the reduced efficiency of cells that produce myelin with age.
Bergles pioneered the study of immature brain cells that can repair myelin after it's destroyed in multiple sclerosis. His work aims to promote myelin repair and restore function for people with MS.
Researchers at OHSU have discovered that a type of herpes virus may be causing a central nervous system disease in monkeys similar to multiple sclerosis in humans. The study found T cells linked to myelin loss, a critical component of MS, paving the way for potential antiviral therapies.
A compound developed at Oregon Health & Science University appears to protect nerve fibers and the fatty sheath of myelin that covers nerve cells. The discovery suggests the compound may also prevent damage from occurring, reducing inflammation and degeneration in multiple sclerosis and other neurodegenerative diseases.
Researchers at the University of Malaga have developed a method to generate human oligodendrocytes from pluripotent stem cells, crucial for supporting neural activity. This breakthrough enables the creation of OLs in just three weeks, opening up new possibilities for treating neurodegenerative diseases such as multiple sclerosis and ALS.
Researchers have developed an immunotherapy approach that specifically impedes the autoimmune response driving MS, while preserving the rest of the immune system. In mouse models, the therapy prevented disease onset and reduced severity after disease onset.
Researchers discovered that N-acetylglucosamine activates myelin stem cells to promote primary myelination and myelin repair. The study suggests that N-acetylglucosamine deficiency may contribute to disease severity in multiple sclerosis patients.
A US researcher has received a National Multiple Sclerosis Society grant to identify compound analogues that can repair damaged axons in multiple sclerosis. The project aims to find a new treatment avenue that speeds up nerve impulses and promotes myelin repair.
Researchers at RIKEN IMS discovered that a combination of gut bacteria worsens multiple sclerosis symptoms in a mouse model. Two specific bacteria, OTU002 and Lactobacillus reuteri, enhance immune cell activity that attacks the brain and spinal cord.
A research team identified a mechanism to control myelin sheath restoration after injury or in multiple sclerosis, regenerating damaged sheaths with theophylline. The study found significant recovery of myelin sheaths in both peripheral and central nervous systems, promoting efficient remyelination.
Researchers at Vanderbilt University Medical Center discovered a cashew shell compound that promotes myelin repair in laboratory experiments. The compound, anacardic acid, inhibits an enzyme involved in gene expression, leading to increased production of IL-33 and rapid induction of myelin genes and proteins.
Researchers have identified a gene, TMEM106B, as a risk factor for neurodegenerative diseases such as Alzheimer's and frontotemporal dementia. The study found that a mutation in this gene disrupts the formation of myelin sheaths around nerve fibers, leading to neurological defects.
Researchers at CU School of Medicine identified microglia's essential role in regulating myelination, a process forming connections between neurons and glial cells. This finding may lead to improved understanding of potential causes for neurological and neuropsychiatric diseases.
Scientists have discovered a new approach to treating Pelizaeus-Merzbacher disease by targeting toxic proteins that prevent myelin production. The treatment, which uses antisense oligonucleotides, reduced symptoms and extended lifespan in laboratory studies.
Scientists uncover role of Rab35 and mTOR signaling pathway in myelin sheath formation, offering potential treatment for CMT4B patients. The study provides new insights into the molecular basis of Charcot-Marie-Tooth disease, a leading inherited neuropathy.
Scientists discovered that patients with certain inflammatory demyelinating diseases have auto-immune antibodies against myelin oligodendrocyte glycoprotein (MOG), which is thought to be important in maintaining the myelin sheath's structural integrity. This finding suggests that therapeutic strategies need to be individualized for pat...
Dr Ian Duncan has made groundbreaking research on how myelin is damaged in multiple sclerosis and how it may be repaired. His work focuses on transplanting myelinating cells to promote function in people with MS.
Researchers have identified a promising new target for multiple sclerosis therapy by focusing on monocytes rather than T and B cells. By targeting the Cxcl10+ monocyte subset, disease symptoms in mice were significantly improved, suggesting potential preventive measures against MS side effects.
Researchers discovered a key role for H2-O chaperone protein in protecting the immune system from autoimmunity, which causes diseases such as multiple sclerosis and rheumatoid arthritis. The study found that the absence of H2-O disrupted normal helper T cell function, leading to autoimmune reactions.
Researchers found that ursolic acid promotes myelin repair in the central nervous system, even in chronic autoimmune disorders like multiple sclerosis. The study suggests a potential dual effect of ursolic acid in treating MS through both immunomodulation and direct remyelination.
A study found that myelin, the protective coating of nerve cells, is dynamic and not inert as traditionally believed. This discovery has implications for treatment of multiple sclerosis and chemobrain, a type of myelin damage caused by chemotherapy drugs.
A study in mice reveals that new nerve insulation, myelin, plays a critical role in laying down long-lasting emotional memories. Increased myelin formation is necessary for the consolidation and maintenance of fear memories, which could lead to new treatments for post-traumatic stress disorder.
A new study reveals that people with autism spectrum disorder (ASD) have a cellular abnormality that impairs production of myelin, a fatty substance that facilitates efficient electrical communication across the brain. This impairment could lead to abnormal brain development and neurological problems associated with ASD.
A new drug called Myeliviz has been approved for its first human trials to aid multiple sclerosis (MS) diagnoses. The drug targets and binds to myelin, allowing for its imaging by a PET scanner, potentially providing earlier and more accurate diagnoses.
A new technique reveals that myelin produces multiple waves of electrical potentials traveling at high speeds, contradicting earlier assumptions. This discovery has significant implications for understanding demyelinating diseases like multiple sclerosis.
Researchers identify Protease Activated Receptor 1 (PAR1) as a molecular switch that promotes myelin regeneration, potentially improving function in neurological disorders. The study's findings suggest new strategies for treating diseases of the central nervous system.
A new study by University of Wisconsin-Madison researchers found that changes in VEP latency can accurately reflect remyelination in multiple sclerosis patients, providing a potential outcome measure for evaluating new treatments.
Researchers used human induced pluripotent stem cells and CRISPR/Cas9 gene editing to model chemical changes in GFAP protein associated with Alexander disease. The study reveals differences in GFAP modifications depending on symptom onset time, allowing for new drug development opportunities.
A study published in GLIA found that myelin impairment causes uncoordinated electrical impulse transmission between neurons, affecting motor learning in mice. The research also showed that compensating for impaired motor learning by pairing actions with brain photo-simulation can promote synchronization of neuronal activities.
Researchers at Oregon Health & Science University have developed a compound that successfully promotes rebuilding of damaged nerve cell protective sheath, reversing MS symptoms. The discovery may lead to clinical trials in humans with MS or other neurodegenerative conditions.
Researchers at Cardiff University have identified the CYFIP1 gene as a potential cause of abnormalities in brain structure seen in psychiatric conditions. The study found that the deletion of this gene leads to thinning of the insulation around nerve cells, disrupting communication between brain regions.
Researchers identify glial cells as critical players in brain's response to social stress. The study found that oligodendrocytes, the myelin-producing cells, play a key role in determining individual resilience or susceptibility to stressful events.
Researchers suggest that viruses hiding in our DNA could be causing some of our deadliest neurological diseases. Studies link HERV reactivation to autoimmune attacks in multiple sclerosis and peripheral demyelinating disease CIDP.
Injured axons trigger Schwann cells to build specialized actin spheres, breaking down and removing damaged fragments to start regeneration. Oligodendrocytes can also generate actin structures with induced VEGFR1 expression, promoting central nervous system healing.
Researchers have discovered that Schwann cells can spread myelin across multiple axons, overturning the traditional understanding of these cells' function. This finding could lead to new gene-therapy techniques to repair damaged myelin in peripheral nervous system disorders like Charcot-Marie-Tooth disease.
A Tel Aviv University study reveals that gene deletion in neurons is responsible for hypersocial behavior in Williams syndrome, caused by myelin sheath deficits. The research also identifies potential treatments using FDA-approved MS drugs.
A scientific breakthrough provides new hope for people with multiple sclerosis, as researchers have developed a compound that stimulates repair of the protective sheath that covers nerve cells in the brain and spinal cord. The study, published in JCI Insight, shows promising results in repairing damaged myelin without severe side effects.
A new University of Rhode Island nursing study found that delayed cord clamping in healthy infants increases iron stores and brain myelin, leading to improved early-life functional development. The study, published in the Journal of Pediatrics, challenges the practice of immediate cord clamping.
A study published in Nature found that people with multiple sclerosis have different types of oligodendrocytes than healthy individuals, which may explain why their myelin repair process does not work as well. This discovery could lead to the development of new treatments for progressive MS.
Researchers found that older cells in MS patients can reform myelin, but new oligodendrocyte generation is severely limited. This suggests treating MS aggressively at an early stage is crucial to prevent further damage.
A team from Charité has identified the Chi3l3 protein as a key player in the body's innate ability to repair damaged myelin sheaths in multiple sclerosis. By understanding this molecular signal, researchers aim to develop new drugs that can restore electrical insulation around nerve cells.
Researchers at Florida State University have discovered that a natural immune system response can cause further harm after a spinal cord injury. The study found that the process of clearing myelin debris from the injury site can lead to inflammation and the formation of abnormal blood vessels, inhibiting recovery.
Researchers at the University of Chicago Medical Center have found a promising treatment for multiple sclerosis, a disabling immune-mediated disease that damages nerve fibers. Sephin1, a small molecule, may delay harm to nerve cells by protecting oligodendrocytes and reducing inflammation.
IDIBELL researchers discovered a novel disease affecting brain white matter in children, caused by DEGS1 gene defect. Fingolimod treatment shows promise in correcting ceramide imbalances and promoting oligodendrocyte survival.