Anacardic acid, a compound found in cashew shells, promotes the repair of myelin. The findings could have positive implications for the treatment of diseases, such as multiple sclerosis, that are characterized by demyelination.
Human iPSCs transplanted into animal models of multiple sclerosis help repair cell damage and restore function.
In late-stage multiple sclerosis, inflammatory cells no longer enter the brain via the bloodstream, but instead the cells arise in memory from local memory cells inside the brain. The findings suggest during the late phases of multiple sclerosis, the disease is occurring entirely inside the brain.
People with schizophrenia have lower levels of S1P, a type of fatty molecule found in white matter. Evaluating post mortem tissue of those who died from a range of psychiatric disorders, researchers found the decreased levels of S1P in the brain was only attributed to those with schizophrenia. The findings could lead to new targeted treatments for the mental health disorder.
Ursolic acid, a compound abundant in fruit peels and some herbs, appears to decrease further neural damage and help regenerate myelin in mouse models of multiple sclerosis. Study reveals ursolic acid suppresses TH17 cells, which are one of the main drivers in the pathological autoimmune response of MS.
The FDA has approved a new drug named Ozanimod for the treatment of multiple sclerosis. Ozanimod binds to receptors in lymphocytes' surfaces, preventing them from reaching the brain. As the number of active lymphocytes decreases, the attack on the immune system diminishes.
Lipids responsible for neural function are highly active and not inert. The findings challenge traditional beliefs about mature myelin.
Postmortem study reveals those with ASD have cellular abnormalities that impair the production of myelin.
Microglia can interfere with macrophages, preventing the movement of these blood immune cells to injury sites. The findings could help in the development of new treatments for multiple sclerosis, Alzheimer's disease, and spinal cord injury.
A new synthetic conduit can bridge large nerve gaps by guiding the regrowth of neurons. When implanted into the arms of macaques with nerve defects in their arms, the conduit boosted neurogenesis and the nerve's ability to conduct signals for a year.
A global knockout of the thrombin receptor PAR1 accelerates myelin development. The findings could help with the development of treatments for diseases associated with demyelination, like multiple sclerosis.
TH17 cells produced increased amounts of SerpinB1, a protein implicated in multiple sclerosis symptoms. SerpinB1 cells were identified with antibodies targeting the CXCR6 surface protein. Using monoclonal antibodies to target CXCR6, the cells disappeared significantly, and the mice primed to develop MS did not develop the disease.
