As the brain ages, microglia adopt dysfunctional states that increase the risk of developing neurodegenerative diseases such as Alzheimer's disease.
CRISPR gene editing created the G795A amino acid which was introduced to microglia derived from human stem cells. Researchers were able to transplant the donor microglia immune cells into humanized rodent models while administering an FDA-approved cancer drug called pexidartinib. The inclusion of the amino acid cause the donated microglia to thrive and resist the drug, while the host microglia died. The findings open the door for new methods of using microglia to treat a range of neurodegenerative disorders.
The Orai1 class of calcium channels regulates sex differences in the functioning of immune cells associated with neuroinflammation and neuropathic pain.
Exposure to drugs that target tauopathies extended survival, reduced neurodegenerative biomarkers, and functionally reduced aberrant behaviors in female mice, but not in males.
High-fat diets promote early inflammatory responses in the brain via an immune pathway associated with diabetes and neurodegenerative diseases. The findings suggest a link between metabolic dysfunction and cognitive impairment.
Researchers have discovered a previously unidentified component of brain anatomy that acts as both a protective barrier and a platform by which immune cells monitor the brain for signs of inflammation and infection.
Reduction of the INPP5D gene variant found in the brain's microglia could help to diminish the risk of late-onset Alzheimer's disease.
Researchers have identified a protein that could be leveraged to help microglia in the brain stave off Alzheimer's and other neurodegenerative diseases.
Researchers have identified two proteins that prevent the formation of scars in the brain and help promote the regeneration of new neural tissue.
Activating TREM2 on microglia in the brains of those with Alzheimer's could help slow down the progression of the neurodegenerative disease.
Deletion of the neurodegenerative disease associated microglial gene CX3CR1 aggravated the disease state and increased the accumulation of plaques in the brains of mouse models of Alzheimer's disease. Deficiencies of the gene also impaired the movement of microglia toward the plaques.
COVID-19 infection causes microglia to excessively engulf synaptic structures and the upregulation of factors involved in phagocytosis.
