@article{0f1f2a26747545e5a2186416ac13a0c8,
title = "Hsp60 Protects against Amyloid β Oligomer Synaptic Toxicity via Modification of Toxic Oligomer Conformation",
abstract = "Alzheimer's disease (AD) is the leading cause of dementia worldwide. While the etiology of AD remains uncertain, neurotoxic effects of amyloid beta oligomers (Aβo) on synaptic function, a well-established early event in AD, is an attractive area for the development of novel strategies to modify or cease the disease's progression. In this work, we tested the protective action of the mitochondrial chaperone Hsp60 against Aβo neurotoxicity, by determining the direct effect of Hsp60 in changing Aβo toxic conformations and thus reducing their dysfunctional synaptic binding and consequent suppression of long-term potentiation. Our data suggest that Hsp60 has a direct impact on Aβo, resulting in a reduction of cytotoxicity and rescue of Aβo-driven synaptic damage, thus proposing Hsp60 as an attractive therapeutic target candidate.",
keywords = "Alzheimer's disease, Amyloid-β oligomers, Hsp60, chaperonin, synaptic plasticity, synaptic toxicity",
author = "Claudia Marino and Balaji Krishnan and Francesco Cappello and Giulio Taglialatela",
note = "Funding Information: *E-mail: gtaglial@utmb.edu. Mailing address: The University of Texas Medical Branch, 10.138D Medical Research Building, 301 University Boulevard, Galveston, TX 77555-1045, USA. ORCID Giulio Taglialatela: 0000-0003-4795-447X Author Contributions C.M. wrote the manuscript, preformed all experiments and the analysis of the results. G.T. contributed to the experimental design of the experiments, the financial support of the experimental work and the preparation of the manuscript. B.K. contributed to the preparation of the manuscript, the electrophysiology experiments and related data analysis. F.C. contributed intellectually to the experimental design and manuscript revision. Funding This work was supported by the Mitchell Center for Neurodegenerative disease and by NIA (National Institute on Aging) research grants (R01AG042890 to GT) and a research grant from the Robert J. Kleberg Jr and Helen C. Kleberg Foundation (to GT). CM and FC were partially supported by the University of Palermo, Italy. Notes The authors declare no competing financial interest. Publisher Copyright: {\textcopyright} 2019 American Chemical Society.",
year = "2019",
month = jun,
day = "19",
doi = "10.1021/acschemneuro.9b00086",
language = "English (US)",
volume = "10",
pages = "2858--2867",
journal = "ACS Chemical Neuroscience",
issn = "1948-7193",
publisher = "American Chemical Society",
number = "6",
}