| First Author | Vossel KA | Year | 2010 |
| Journal | Science | Volume | 330 |
| Issue | 6001 | Pages | 198 |
| PubMed ID | 20829454 | Mgi Jnum | J:164887 |
| Mgi Id | MGI:4835593 | Doi | 10.1126/science.1194653 |
| Citation | Vossel KA, et al. (2010) Tau reduction prevents Abeta-induced defects in axonal transport. Science 330(6001):198 |
| abstractText | Amyloid-beta (Abeta) peptides, derived from the amyloid precursor protein, and the microtubule-associated protein tau are key pathogenic factors in Alzheimer's disease (AD). How exactly they impair cognitive functions is unknown. We assessed the effects of Abeta and tau on axonal transport of mitochondria and the neurotrophin receptor TrkA, cargoes that are critical for neuronal function and survival and whose distributions are altered in AD. Abeta oligomers rapidly inhibited axonal transport of these cargoes in wild-type neurons. Lowering tau levels prevented these defects without affecting baseline axonal transport. Thus, Abeta requires tau to impair axonal transport, and tau reduction protects against Abeta-induced axonal transport defects. |
