Synapses, Microglia, and Lipids in Alzheimer’s Disease

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...

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Published inFrontiers in neuroscience Vol. 15; p. 778822
Main Authors Paasila, Patrick J., Aramideh, Jason A., Sutherland, Greg T., Graeber, Manuel B.
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 12.01.2022
Frontiers Media S.A
Subjects
Alzheimer's disease
APOE
Apolipoprotein E
Autopsy
Brain
Central nervous system
Dementia
Dystrophy
Gene expression
Lipid metabolism
Lipids
Metabolism
Microglia
Myeloid cells
Neurodegenerative diseases
Neuronal-glial interactions
Neuroscience
Peptides
Proteins
synapses
TREM2
lipids
TREM2
synapses
APOE
Alzheimer’s disease
microglia
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Summary: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.
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Reviewed by: Dan Frenkel, Tel Aviv University, Israel; Gareth R. Howell, The Jackson Laboratory, United States
Edited by: Bente Finsen, University of Southern Denmark, Denmark
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
ISSN:1662-453X
1662-4548
1662-453X
DOI:10.3389/fnins.2021.778822