| First Author | Stokin GB | Year | 2005 |
| Journal | Science | Volume | 307 |
| Issue | 5713 | Pages | 1282-8 |
| PubMed ID | 15731448 | Mgi Jnum | J:96346 |
| Mgi Id | MGI:3530194 | Doi | 10.1126/science.1105681 |
| Citation | Stokin GB, et al. (2005) Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease. Science 307(5713):1282-8 |
| abstractText | 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. |
