Synapses, Microglia, and Lipids in Alzheimer's Disease.

Autor: Paasila PJ; Charles Perkins Centre, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia.; School of Medicine, Western Sydney University, Campbelltown, NSW, Australia., Aramideh JA; Brain and Mind Centre, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia., Sutherland GT; Charles Perkins Centre, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia., Graeber MB; Brain and Mind Centre, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia.
Jazyk: angličtina
Zdroj: Frontiers in neuroscience [Front Neurosci] 2022 Jan 12; Vol. 15, pp. 778822. Date of Electronic Publication: 2022 Jan 12 (Print Publication: 2021).
DOI: 10.3389/fnins.2021.778822
Abstrakt: Alzheimer's disease (AD) is characterised by synaptic dysfunction accompanied by the microscopically visible accumulation of pathological protein deposits and cellular dystrophy involving both neurons and glia. Late-stage AD shows pronounced loss of synapses and neurons across several differentially affected brain regions. Recent studies of advanced AD using post-mortem brain samples have demonstrated the direct involvement of microglia in synaptic changes. Variants of the Apolipoprotein E and Triggering Receptors Expressed on Myeloid Cells gene represent important determinants of microglial activity but also of lipid metabolism in cells of the central nervous system. Here we review evidence that may help to explain how abnormal lipid metabolism, microglial activation, and synaptic pathophysiology are inter-related in AD.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2022 Paasila, Aramideh, Sutherland and Graeber.)
Databáze: MEDLINE
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