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Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) in transgenic mouse models of frontotemporal lobar degeneration and Alzheimer’s disease

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Translational Neurodegeneration 2013年第1期2卷 174-182页

作者： Shuk Wai Ho Yuk Tung Chanel Tsui Ting Ting Wong stanley kwok-kuen cheung William B Goggins Lau Ming Yi kwok Kin Cheng Larry Baum Department of Surgery The University of Hong KongPokfulamHong KongChina School of Biomedical Sciences(Pharmacology) The University of NottinghamNottinghamUK Department of Microbiology The University of Hong KongPokfulamHong KongChina School of Public Health and Primary Care The Chinese University of Hong KongShatinHong KongChina School of Pharmacy The Chinese University of Hong KongShatinHong KongChina

Alzheimer’s disease(AD),the most common dementia,is characterized by potentially neurotoxic aggregation of Aβ peptide and tau protein,and their deposition as amyloid plaques and neurofibrillary tangles(NFTs).Tau aggregation also occurs in other common neurodegenerative *** dementia(FTD)can be caused by tau mutations that increase the susceptibility of tau to hyperphosphorylation and aggregation,which may cause neuronal dysfunction and deposition of NFTs.17-allylamino-17-demethoxygeldanamycin(17-AAG)is a potent inhibitor of heat shock protein 90(Hsp90),a cytosolic chaperone implicated in the proper folding and functions of a repertoire of client proteins.17-AAG binds to Hsp90 and enhances degradation of Hsp90 client *** sought to determine whether 17-AAG can reduce Aβ and tau pathology in the brains of AD and FTD model mice expressing Aβ or P301L mutant tau,*** were randomized to receive 25,5,or 0 mg/kg 17-AAG thrice weekly from age eight to 11 *** was performed by rotarod test on motor function,on the area occupied by plaques in hippocampus or NFTs in medulla tissue sections,and on mortality.A high dose of 17-AAG tended to decrease NFTs in male mice(p=0.08).Further studies are required to confirm the effect of 17-AAG in diseases of tau aggregation.

关键词： Dementia Mouse Tangles Plaques

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