Abstract
Microglia, the primary immune cells of the central nervous system, hold a multitude of tasks in order to ensure brain homeostasis and are one of the best predictors of biological age on a cellular level. We and others have shown that these long-lived cells undergo an aging process that impedes their ability to perform some of the most vital homeostatic functions such as immune surveillance, acute injury response, and clearance of debris. Microglia have been described as gradually transitioning from a homeostatic state to an activated state in response to various insults, as well as aging. However, microglia show diverse responses to presented stimuli in the form of acute injury or chronic disease. This complexity is potentially further compounded by the distinct alterations that globally occur in the aging process. In this review, we discuss factors that may contribute to microglial aging, as well as transcriptional microglia alterations that occur in old age. We then compare these distinct phenotypic changes with microglial phenotype in neurodegenerative disease.
Highlights
Microglia originate from hematopoietic progenitor cells found in the yolk sac and, upon entering the brain, gradually adapt a homeostatic microglial phenotype [1]
Microglia with transcriptomic signatures consistent with that found in neurodegenerative diseases represent only a minority of microglia in healthy aging
It remains unclear what this subset of microglia contributes toward overall microglial dysfunction or, if they might have a beneficial impact
Summary
Institute of Cell Biology and Neuroscience, Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Frankfurt am Main, Germany Edited by: Gabor Petzold, Helmholtz Association of German Research Centers (HZ), Germany Reviewed by: Karen Gertz, Charité – Universitätsmedizin Berlin, Germany Sabina Tahirovic, Helmholtz Association of German Research Centers (HZ), Germany
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