Microglia communication: Parallels between aging and Alzheimer's disease
| Autor: | Joe C. Udeochu, Saul A. Villeda, Jeremy M. Shea |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Focused review series on neuroinflammation in neurodegeneration Immunology Neuroscience (miscellaneous) microglia Review Article Disease neuroinflammation 03 medical and health sciences 0302 clinical medicine Immune system Immunology and Microbiology (miscellaneous) medicine Review Articles Neuroinflammation Microglia aging Cognition Phenotype 030104 developmental biology medicine.anatomical_structure Synaptic plasticity alzheimer's disease Neurology (clinical) Psychology Neuroscience 030217 neurology & neurosurgery Homeostasis |
| Zdroj: | Clinical & Experimental Neuroimmunology |
| ISSN: | 1759-1961 |
| DOI: | 10.1111/cen3.12307 |
| Popis: | Aging alters the functional integrity of the adult brain, driving cognitive impairments and susceptibility to neurodegenerative disorders in healthy individuals. In fact, aging remains the most dominant risk factor for Alzheimer's disease (AD). Recent findings have expanded our understanding of microglia function in the normal aging and AD brain, provoking an appreciation for microglia involvement in remodeling neuronal connections and maintaining brain integrity. This homeostatic function of microglia is achieved in part through the ability of microglia to interact extensively with and rapidly respond to changes in the brain microenvironment to enable adequate phenotypic transformations. Here, we discuss pro‐inflammatory drivers of microglia transformation in aging and AD by focusing on the immune‐modulatory functions of secreted factors, such as cytokines, complement factors and extracellular vesicles. We highlight the involvement of these secreted factors in aging and AD‐associated cellular changes in microglia immune activation, surveillance function, and phagocytosis. Finally, we discuss how pro‐inflammatory phenotypic changes associated with altered immune communication could both facilitate and exacerbate impairments in synaptic plasticity and cognitive function observed in the aged and AD brain. |
| Databáze: | OpenAIRE |
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