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.
Opioid use disorder affects genes associated with proinflammatory immune molecule encoding and genes associated with remodeling the extracellular matrix, suggesting the connection between neurons may be altered as a result of opioid use. Additionally, those with OUD have higher levels of microglia in the brain.
Aromatic turmerone, a compound derived from turmeric essential oil, and its derivatives directly affect dopamine neurons to generate neuroprotective properties in tissue culture models of Parkinson's disease.
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.
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.
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.