期刊
SCIENCE
卷 330, 期 6001, 页码 198-U52出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1194653
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资金
- NCRR NIH HHS [C06 RR018928] Funding Source: Medline
- NIA NIH HHS [R37 AG011385, R01 AG011385-07, AG011385, R01 AG011385] Funding Source: Medline
- NINDS NIH HHS [R00 NS057906, R01 NS041787-09, R00 NS057906-05, R01 NS041787, NS041787, K99 NS057906, NS057906] Funding Source: Medline
Amyloid-beta (A beta) 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 A beta 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. A beta oligomers rapidly inhibited axonal transport of these cargoes in wild-type neurons. Lowering tau levels prevented these defects without affecting baseline axonal transport. Thus, A beta requires tau to impair axonal transport, and tau reduction protects against A beta-induced axonal transport defects.
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