CYFIP1 plays a key role in the damaging effects of 15q11.2 deletion. When CYFIP1 is missing, myelin abnormalities occur. The findings shed light on how psychiatric disorders, such as schizophrenia and autism, may develop.
The behavior of oligodendrocytes plays a critical role in determining whether we tolerate or succumb to stress.
Senolytic drugs administered to mice reduced senescent cells around amyloid plaques by more than 90% and decreased neuroinflammation by 50%. Mice treated with the drug combination also showed improvements in spatial memory, compared to other Alzheimer's model mice who received no treatment. The findings could have positive implications for the treatment of Alzheimer's disease in people with the condition.
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Axon myelination is significantly disrupted in patients with Alzheimer's disease. Researchers also found brain cells of men and women vary significantly in how their genes respond to the neurodegenerative disease.
Myelin thickness and oligodendrocytes were significantly reduced in the prefrontal cortex in mouse models of Williams syndrome.
A study in mouse models of multiple sclerosis demonstrates a compound called sobetirome promotes remyelination, and a derivative of the compound can penetrate the blood-brain barrier to enable a tenfold increase in infiltration to the CNS. Researchers are confident their research will translate from mice into humans, providing a new avenue of treatment for MS.
Dysregulation of Zfp36l1 causes neural lineage progenitor cells to grow rapidly, taking on the properties of fast growing stem cells as they become cancerous.
Researchers have successfully created stem cell derived brain cells which can generate oligodendrocytes, neurons and astrocytes.
A new study sheds light on brain cells implicated in multiple sclerosis. Researchers found there are several types of oligodendrocytes, and the ratio of these cells differ significantly in those with MS. The findings could help develop new targeted treatments for progressive multiple sclerosis.
Researchers have discovered how the body is able to initiate repair mechanisms which can limit the extent of damage to the myelin sheath. The findings could help with the development of new therapies for multiple sclerosis.
Researchers discover the protein nestin produced in astrocytes plays a role in inhibiting neural differentiation. The study reports nestin does not control adult neurogenesis by acting within neural stem cells, but by regulating Notch signals neural stem cells receive from astrocytes.
Study reveals PRRX1 gene expression results in cell cycle arrest and quiescence of oligodendrocyte progenitors, blocking myelin production.