Dendritic spine loss and synaptic alterations in Alzheimer's disease.
Dendritic spines are tiny protrusions along dendrites, which constitute major postsynaptic sites for excitatory synaptic transmission. These spines are highly motile and can undergo remodeling even in the adult nervous system. Spine remodeling and the formation of new synapses are activity-dependent processes that provide a basis for memory formation. A loss or alteration of these structures has been described in patients with neurodegenerative disorders such as Alzheimer's disease (AD), and in mouse models for these disorders. Such alteration is thought to be responsible for cognitive deficits long before or even in the absence of neuronal loss, but the underlying mechanisms are poorly understood. This review will describe recent findings and discoveries on the loss or alteration of dendritic spines induced by the amyloid beta (Abeta) peptide in the context of AD.
Knobloch
Marlen
M
Division of Psychiatry Research, University of Zurich, 8008 Zurich, Switzerland.
Mansuy
Isabelle M
IM
D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003599:Cytoskeleton / Q000378:metabolism / Q000473:pathology; D049229:Dendritic Spines / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013569:Synapses / Q000378:metabolism / Q000473:pathology*; D009435:Synaptic Transmission / Q000502:physiology
D016229:Amyloid beta-Peptides