Neuroinflammation may be a key player in the pathological brain changes produced as a result of chronic opioid use. Microglia is likely responsible for the majority of the changes.
A new model of Alzheimer's progression highlights the link between glial cells, toxic protein buildup, and neurodegeneration.
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.
Secondary infections and novel inflammatory events, even ones that occur external to the brain, amplify the brain's immune response and detrimentally impact cognition in mouse models of Alzheimer's disease.
Study identifies gene expression signatures that underlie microglia associated with amyloid plaque phagocytosis.
Sevoflurane, an anesthetic, causes tau to leave neurons and enter microglia. This stimulates the production of interleukin-6, leading to inflammation and cognitive impairment.
Microglia creates dense-core plaques which help to clear away more wispy plaques from neurons, preventing cell death. Findings suggest the dense-core plaques play a defensive role in protecting the brain from the ravages of neurodegenerative diseases, such as Alzheimer's.
A new drug modulates, rather than inhibits, a key enzyme implicated in the formation of Alzheimer's related plaques.
Microglia are essential for pruning away extra neural connections in the development of the auditory brainstem.
Microglia appear to play a key role in inflammation-associated depression.
Disruptions in circulating white blood cells may be a key driver in ALSP, a rare form of early-onset dementia.
Changes in fetal microglia caused as a result of maternal inflammation could contribute to the development of schizophrenia, autism, and other psychiatric or developmental disorders.
