Articles tagged with Myelin Sheath
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Researchers have identified a mechanism to regenerate insulating layers in the brain that protect nerve fibers in multiple sclerosis. The study shows activating stem cells can repair injury in the central nervous system, reversing damage caused by MS.
Researchers at Purdue University have found evidence that acrolein, an environmental toxin, may play a key role in causing multiple sclerosis. They also discovered that the hypertension drug hydralazine can delay disease onset and reduce symptoms by neutralizing acrolein.
A team of researchers at Tel Aviv University has developed genetically mutated mice to study Vanishing White Matter disease, which destroys brain myelin. The new tool allows for the first time to follow the exact process of myelin destruction, providing valuable information about the molecular mechanisms of the disease.
Researchers at Stanford University School of Medicine have discovered that antibodies are critical to the repair of nerve damage in the peripheral nervous system. In a new study, scientists show that certain antibodies can facilitate myelin clearance and nerve regeneration, while others do not.
Research reveals a mechanism for autoimmune disease that depends on killer T cells expressing dual receptors for normal proteins and pathogens. The study found that viruses lacking the specific protein can still trigger the disease, suggesting a complex interplay between viral infections and genetic predisposition.
Researchers at the University of California, San Diego School of Medicine found that removing three key inhibitory molecules from myelin did not significantly improve axon regeneration in damaged spinal cords. The study suggests that successful regeneration will require a combination of many approaches and techniques.
Researchers at UCF are exploring new ways to potentially reverse the damage caused by multiple sclerosis and other neurological disorders. The team will study the breakdown of myelin, a substance that coats and protects nerves, with the goal of developing new drugs that can reverse the damage and improve patient outcomes.
Researchers used a special peptide to modify laboratory mice's immune systems, reducing characteristic features of Alzheimer's disease. Anti-inflammatory cells were recruited, dampening the local inflammatory response and boosting plaque-degrading enzyme action.
Researchers from Boston College have made a significant discovery about myelin structure and stability using x-ray diffraction. They found that early protein processes are crucial to the proper formation and layering of the myelin membrane, which is critical for nerve conduction and nervous system function.
Researchers at Thomas Jefferson University found that fractionated stereotactic radiotherapy is effective in controlling optic nerve sheath meningioma growth while preserving vision. The treatment resulted in a high rate of stabilized or improved visual acuity, with minimal late complications.
Researchers propose a new hypothesis for Alzheimer's disease: the myelin model. This theory suggests that degenerative diseases like Alzheimer's begin with normal brain maintenance and repair processes. The model suggests targeting earlier stages of myelination, potentially reducing dementia's burden.
The model system will help understand causes of myelin-related conditions, such as diabetic neuropathy and multiple sclerosis. Researchers plan to use the new model to explore origins of diabetic neuropathy and test new drug therapies.
Researchers at the University of Cambridge and UCSF have identified the Wnt pathway as a crucial determinant of brain stem cells' ability to repair damaged tissue. The study's findings open up new avenues for developing therapies that block the Wnt pathway, potentially enhancing remyelination in MS patients.
Researchers found that biochemical signals inhibit oligodendrocyte development, hindering myelin repair in multiple sclerosis. The Wnt pathway's role in myelin production and repair has been identified as a key factor in the disease's progression.
Researchers at McGill University found that statin therapy can inhibit myelin repair in Multiple Sclerosis patients. The study suggests a negative impact of long-term statin therapy on remyelination and oligodendrocyte number.
Researchers at Medical College of Georgia have identified a critical protein called erbin that regulates insulation in the peripheral nervous system. Impaired myelin formation is linked to neurological and psychiatric diseases, while erbin's role in cancer therapy provides a potential new site for targeted treatment.
Multiple sclerosis researchers discover that the immune system targets gray matter in addition to myelin, damaging nerve cell bodies and leading to irreversible destruction of axons. The newly identified protein Contactin-2 plays a critical role in this process.
Researchers from the University of Wisconsin successfully generated human embryonic stem cells that can produce myelin, a finding with potential for both basic and clinical research. The process takes 14 weeks compared to 2 weeks for mouse ES cells.
Scientists studying a mysterious neurological affliction in cats discovered a key ability of the central nervous system to repair itself. Recovery was achieved through remyelination, where previously demyelinated axons became restored with thin but functional myelin sheaths.
A new study identifies miR-23 as a microRNA that regulates myelin formation and maintenance. By turning down lamin gene expression, miR-23 prevents demyelination due to lamin overexpression, offering a potential treatment for demyelinating illnesses.
Researchers found that claudin 11 prevents charged ion leakage through myelin layers, increasing resistance and affecting signal conduction. This defect may be linked to cognitive deficits and neurodegenerative diseases, particularly in neurons with thin myelin sheaths.
Researchers created a genetically modified mouse expressing excessive PAD2, resulting in significant myelin loss and behavioral deficits. The study highlights PAD as a potential therapeutic target and marker for early detection of MS and related diseases.
Researchers found a correlation between motor task performance and myelin integrity, peaking in middle age before declining. Myelin breakdown may underlie cognitive decline and physical skills erosion, but therapeutic interventions could slow the process.
A new marker for raised intracranial pressure has been identified using magnetic resonance imaging measurements of the optic nerve sheath. A retro-bulbar optic nerve sheath diameter above 5.82mm predicts raised ICP in 90% of cases, providing a non-invasive solution for early detection and treatment.
The Montel Williams MS Foundation has awarded $325,000 in research grants to seven institutions studying new treatments for multiple sclerosis, including methods for early detection and restoring depleted myelin. The foundation aims to advance knowledge that will lead to more effective diagnosis and treatment of the disease.
Researchers at UT Southwestern Medical Center found that giving infants and children 100% oxygen after a brain injury can cause more harm than good. The study suggests that brief exposure to 100% oxygen during resuscitation worsens white-matter injuries, leading to increased brain-cell death and coordination problems.
Researchers used human stem cells to repair defective wiring in the brain and spinal cord of mice with a neurological condition similar to fatal childhood diseases. The treatment showed promising results, with four mice appearing completely cured and six living far beyond their usual lifespan.
Researchers found that activating the c-Jun gene in cultured neurons with Schwann cells promotes dedifferentiation and speeds nerve healing. The study suggests a new potential target for understanding and treating diseases like Charcot-Marie Tooth disease and Guillain-Barre syndrome.
Researchers at Mayo Clinic have discovered an antibody that can repair the damaged myelin sheath in laboratory mouse models, a crucial step towards treating multiple sclerosis and related disorders. The antibody promotes remyelination with a single dose, paving the way for potential new treatments.
Stephen A. Back, a pediatric neurology expert at Doernbecher Children's Hospital, has received the prestigious Javits Neuroscience Investigator Award for his research on white matter brain injury in premature infants. His work aims to develop therapies that can reverse brain damage and slow cognitive decline in aging adults.
Purdue researchers used CARS imaging to study how the myelin sheath is degraded by lysophosphatidylcholine. The findings suggest that calcium ions activate enzymes that break down proteins and molecules in the myelin, leading to its degradation. This research may lead to new treatments for multiple sclerosis.
Researchers found a pair of proteins that facilitate communication between axons and glial cells, initiating myelination. Understanding this process may lead to new treatments for neurodegenerative diseases like MS.
Researchers at Stanford University School of Medicine have identified alphaB-crystallin as a protective protein that plays a critical role in multiple sclerosis. The protein, normally found in the lens of the eye, can reverse paralysis and suppress inflammation in mice, suggesting a potential therapeutic application.
Researchers found that a breakdown of myelin in the developing brain may contribute to the progression of Huntington's disease. The study, led by Dr. George Bartzokis at UCLA, suggests that an abnormality in the Htt gene affects myelin nourishment, leading to neuron death and disease symptoms.
Researchers propose a new mechanism for Alzheimer's disease, linking breakdown of myelin to amyloid-beta fibrils and neurodegeneration. Myelination is key to brain function, and its decline with age may underlie the disease's progression.
In a groundbreaking discovery, Johns Hopkins scientists found that brain cells in the white matter communicate through electrical signals similar to those used by gray matter cells. This process allows 'naked' nerve cells to signal nearby oligodendrocyte precursor cells, potentially aiding in the repair of damaged myelin coats.
Researchers developed a combined imaging method using three microscopic techniques to study the molecular mechanisms of multiple sclerosis. The technique enables the analysis of living tissue, revealing details about astroglial filaments and myelin sheath degradation, which could lead to earlier detection and new treatments.
A defect in one copy of the EGR2 gene disrupts myelin production, leading to peripheral neuropathy. Researchers have deciphered a key sequence essential to myelin assembly, paving the way for new therapies.
A fibrous protein called fibrinogen promotes multiple sclerosis (MS) when it leaks into the brain, triggering inflammation. Researchers at UCSD have identified a specific receptor that binds to fibrinogen and inhibit this inflammation process.
Macrophages play a critical role in clearing debris after nerve damage, but their continued presence can damage tissue and compromise repair. Now, researchers have identified a process that allows macrophages to be cleared, enabling nerve regeneration.
Researchers discover that pregnancy-related hormone prolactin encourages spontaneous production of myelin, a fatty substance coating nerve cells, potentially leading to treatment for MS. Prolactin therapy aims to promote repair and improve symptoms in people with MS.
Researchers at U of MN have discovered a treatment to halt disease progression in advanced ALD patients by combining NAC and transplant. This breakthrough offers new hope for devastating disease affecting young boys.
Researchers have identified a molecule, osteopontin, that plays a central role in relapses of autoimmune diseases such as multiple sclerosis, lupus, and rheumatoid arthritis. Osteopontin promotes the survival of T cells that carry out the damaging attack on myelin, increasing their destructive potential.
A new study proposes that myelin, the fatty insulation around brain cells, is linked to various neuropsychiatric disorders such as schizophrenia and Alzheimer's. The research suggests that enhancing myelination through cholinergic treatments may improve neuron signaling and potentially delay disease progression.
Vanderbilt researchers have successfully produced movies that provide the first direct view of the initial stage of myelin sheath formation in nerves. The process is more dynamic than previously thought, with cells continually sending out tiny tentacles to readjust their positions.
A USC study has identified a crucial protein involved in the formation of myelin, which could lead to new treatments for conditions such as multiple sclerosis. The research discovered that a protein called Par-3 plays a central role in regulating myelination by interacting with other molecules.
A new study has shed light on the mechanisms controlling myelin formation, a process crucial for efficient nerve communication. Researchers found that Par-3 acts as a molecular scaffold to organize key proteins essential for myelination.
A new study found that variations of the OLIG2 gene are strongly associated with schizophrenia. The gene plays a crucial role in myelin production and is coordinated with other genes involved in myelination and schizophrenia development. This causal link may help researchers develop new therapeutic targets for the debilitating illness.
Researchers discovered that astrocytes promote myelination by releasing leukemia inhibitory factor (LIF) in response to electrical impulses. This finding may lead to new treatments for demyelinating diseases, such as multiple sclerosis.
A recent study published in Archives of General Psychiatry found a significant link between genetic risk factors and myelin breakdown in the brain. The research suggests that assessing myelin health through MRI may help identify individuals at risk for Alzheimer's disease, allowing for targeted prevention strategies.
A UW-Madison study finds that defective cells can be reinvigorated by replacing a missing enzyme, allowing the healthy maintenance of myelin. The research provides proof of principle for a new therapeutic strategy to treat Krabbe's disease and other inherited demyelinating diseases.
Researchers have identified two proteins found in the Neurofascin gene that link glial ensheathment of nerve fibers to node formation. This breakthrough discovery may help find ways to improve nerve conduction in patients with conditions like MS.
Research suggests that disruption of myelination is a key component behind childhood developmental disorders such as autism, ADHD, and schizophrenia. Incomplete inhibitory circuits may lead to impulsive behaviors, while fully functional excitatory circuits worsen psychiatric disorders.
Researchers at Yale University found that myelin physically limits axonal growth and regeneration after traumatic injury. Blocking vision in one eye normally alters ocular dominance only during critical development, but mutations in the Nogo-66 receptor affect abnormal plasticity later in life.
Researchers at Yale University have developed two ways to induce MS symptoms in mice, revealing a key distinction between disease-causing and non-disease antibodies. The study brings the team closer to pinpointing accurate diagnostic tools for individual MS patients.
Researchers identify neuregulin gene as key factor in myelin production, enabling faster neural transmission. The discovery opens possibilities for repairing damaged spinal cords and brain tracts.
Researchers at UW-Madison are developing cell transplant techniques to repair damaged myelin and protect nerve fibers in multiple sclerosis. The $3.4 million grant will support the use of human stem cells and minocycline, an antibiotic with anti-inflammatory properties.
Researchers identify signal in damaged brain that prevents cells from restoring lost myelin; HA accumulation linked to CD44 protein. Oligodendrocyte progenitors can be prevented from maturing into myelin-producing cells, while injection of HA into damaged myelin prevents reforming.
Researchers at UT Southwestern Medical Center have identified ephrin-B3 as a molecule that inhibits the regrowth of spinal nerve cells. The study found that ephrin-B3, which normally helps control nerve fiber growth during embryonic development, is also present in high levels in adult myelin and blocks neuron regeneration.
Research reveals significant decreases in myelin lipid synthesis in mice with Canavan disease, suggesting a link between acetate deficiency and the disorder. The findings support the potential of acetate supplementation as a therapy for this devastating congenital disease.