期刊
SCIENCE
卷 307, 期 5713, 页码 1282-1288出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1105681
关键词
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资金
- NEI NIH HHS [EY13408, R01 EY007042-19, EY12598, R01 EY007042, R01 EY013408, R01 EY013408-02] Funding Source: Medline
- NIA NIH HHS [P50 AG05131] Funding Source: Medline
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-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.
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