Synapses, Microglia, and Lipids in Alzheimer’s Disease

Frontiers in Neuroscience

Neuroscience

Jason A. Aramideh¹  Manuel B. Graeber¹  Greg T. Sutherland²  Patrick J. Paasila³ 

[1] Brain and Mind Centre, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia;Charles Perkins Centre, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW, Australia;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;

关键词: Alzheimer’s disease;    APOE;    lipids;    microglia;    synapses;    TREM2;   

DOI  :  10.3389/fnins.2021.778822

 received in 2021-09-17, accepted in 2021-12-06,  发布年份 2022

来源: Frontiers

【 摘 要 】

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.

【 授权许可】

Unknown   
Copyright © 2022 Paasila, Aramideh, Sutherland and Graeber.

【 图 表 】

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