Neuronal structure is altered by amyloid plaques.
During the course of Alzheimer's disease (AD), neurons undergo extensive remodeling, contributing to the loss of function observed in the disease. Many brain regions in patients with AD show changes in axonal and dendritic fields, dystrophic neurites, synapse loss, and neuron loss. Accumulation of amyloid-beta protein, a pathological hallmark of the disease, contributes to many of these alterations of neuronal structure. Areas of the brain displaying a high degree of plasticity are particularly vulnerable to degeneration in Alzheimer's disease. This article describes neuronal changes that occur in AD, reviews evidence that amyloid-beta contributes to these changes, and finally discusses the recovery of amyloid-induced changes in the brains of transgenic mice, lending hope to the idea that therapeutic strategies which reduce amyloid-beta production will lead to functional recovery in patients with AD.
Spires
Tara L
TL
Department of Neurology, Alzheimer's Disease Research Laboratory, Massachusetts General Hospital, Charlestown, MA 02129, USA. tspires@partners.org
Hyman
Bradley T
BT
D000544:Alzheimer Disease / Q000473:pathology* / Q000628:therapy; D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D030801:Animals, Genetically Modified; D001369:Axons / Q000502:physiology; D049229:Dendritic Spines / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D007167:Immunotherapy / Q000379:methods; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D058225:Plaque, Amyloid / Q000502:physiology*; D013569:Synapses / Q000473:pathology / Q000502:physiology
D016229:Amyloid beta-Peptides