Synaptic Loss in Alzheimer's Disease: Mechanistic Insights Provided by Two-Photon in vivo Imaging of Transgenic Mouse Models

Synapse loss is the strongest correlate for cognitive decline in Alzheimer's disease. The mechanisms underlying synapse loss have been extensively investigated using mouse models expressing genes with human familial Alzheimer's disease mutations. In this review, we summarize how multiphoto...

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Published in:Frontiers in cellular neuroscience 2020-12, Vol.14, p.592607
Main Authors: Subramanian, Jaichandar, Savage, Julie C, Tremblay, Marie-Ève
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amyloid
amyloid mouse models
Animal models
Brain
Calcium homeostasis
Cellular Neuroscience
Cognitive ability
dendritic spines
in vivo imaging
Microglia
Microscopy
Morphology
Mutation
Neurodegenerative diseases
Neuroimaging
Pathology
Proteins
Rodents
Transgenic mice
two-photon
Visualization
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Savage, Julie C
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description Synapse loss is the strongest correlate for cognitive decline in Alzheimer's disease. The mechanisms underlying synapse loss have been extensively investigated using mouse models expressing genes with human familial Alzheimer's disease mutations. In this review, we summarize how multiphoton imaging has improved our understanding of synapse loss mechanisms associated with excessive amyloid in the living animal brain. We also discuss evidence obtained from these imaging studies for the role of cell-intrinsic calcium dyshomeostasis and cell-extrinsic activities of microglia, which are the immune cells of the brain, in mediating synapse loss.
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subjects Alzheimer's disease
Amyloid
amyloid mouse models
Animal models
Brain
Calcium homeostasis
Cellular Neuroscience
Cognitive ability
dendritic spines
in vivo imaging
Microglia
Microscopy
Morphology
Mutation
Neurodegenerative diseases
Neuroimaging
Pathology
Proteins
Rodents
Transgenic mice
two-photon
Visualization
title Synaptic Loss in Alzheimer's Disease: Mechanistic Insights Provided by Two-Photon in vivo Imaging of Transgenic Mouse Models
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