A molecular process caused by the TREM2 gene mutation in the brain's microglia increases the risk of Alzheimer's disease, a new study reports.
A new study in mice finds microglia help neurons grow synapses critical for cognitive function.
A study of monozygotic twins allowed researchers to discover which parts of immune dysfunction in multiple sclerosis were influenced by genetics, and which were influenced by environmental factors.
Microglia, a key immune cell in the brain, appears to mediate the relationship between the gut microbiome and amyloid-beta deposits in male mouse models of Alzheimer's disease.
A drug currently being tested in cancer clinical trials appears to prevent dysfunction in an immune cell signaling pathway associated with Alzheimer's disease. Blocking the pathway could prevent Alzheimer's from developing and slow the progression of symptoms for those who already have the disease.
In fruit flies, there is a second barrier in the brain where glial cells ensure a spatial separation for different functional compartments.
Analyzing the gene activity of 66,000 cells from human brain tissue, researchers generated a comprehensive map of cell types associated with brain lesions in multiple sclerosis, and their gene expression patterns and interactions.
Sustained microglia activation leads to the cells becoming senescent. This leads to an accelerated accumulation of amyloid in the brain, influencing the early stages of Alzheimer's development.
Immune cells in the meninges come from bone marrow in the skull and migrate to the brain through special channels without passing through the blood. These immune cells help to guard the brain and spinal cord against inflammation and infection.