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Axonopathy and Transport Deficits Early in the Pathogenesis of Alzheimer's Disease
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Axonopathy and Transport Deficits Early in the Pathogenesis of Alzheimer's Disease
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Journal Article
Axonopathy and Transport Deficits Early in the Pathogenesis of Alzheimer's Disease
2005
Overview
We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-{szligbeta} peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of {szligbeta}-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
/ Alzheimer Disease - genetics
/ Alzheimer Disease - metabolism
/ Alzheimer Disease - pathology
/ amyloid
/ Amyloid beta-Peptides - metabolism
/ Amyloid beta-Protein Precursor - metabolism
/ Amyloids
/ Animals
/ Axons
/ Basal Nucleus of Meynert - pathology
/ Biological and medical sciences
/ Brain
/ Cytoplasmic Vesicles - ultrastructure
/ Female
/ Humans
/ kinesin
/ Male
/ Mice
/ Microtubule-Associated Proteins - genetics
/ Microtubule-Associated Proteins - metabolism
/ Neurites
/ Swelling
