Infection Drives Microglia Into Inflammatory Behavior that Contributes to Neurodegeneration

Correlations have been found between infectious disease and incidence of neurodegenerative conditions. The dominant hypothesis is that microglia, innate immune cells of the brain, are made more inflammatory by infection, and the resulting chronic inflammation in brain tissue produces dysfunction that contributes to neurodegeneration. The role of microglia in the onset and progression of neurodegenerative conditions is studied more generally as well, as these cells react to signs of damage in aging tissue in much the same way as they react to infection. Further, microglia also enter a state of cellular senescence in increasing numbers with age, becoming highly pro-inflammatory. A sizable fraction of senescent microglia can be removed by senolytic treatments that pass the blood-brain barrier, such as the dasatinib and quercetin combination, and this has shown benefits in animal models of neurodegeneration. Equally, microglia can be cleared completely from the brain by blocking CSF1R. A new population of microglia is produced and replaces the old within a few weeks, lacking the damage and dysfunction of their predecessors. This too has been shown to produce benefits in animal models of neurodegeneration. Microglial Priming in Infections and Its Risk to Neurodegenerative Diseases Infections of different etiologies, neurotropic or not, have been associated with acute and long-term neurological consequences. These consequences involve cognitive decline and be...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs