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Issue title: Alzheimer’s Disease: New Beginnings
Guest editors: G. Perry, J. Avila, P.I. Moreira, A.A. Sorensen and M. Tabaton
Article type: Review Article
Authors: Martini, Alessandra C.a; * | Forner, Stefaniaa | Trujillo-Estrada, Lauraa | Baglietto-Vargas, Davida | LaFerla, Frank M.a; b; *
Affiliations: [a] Institute for Memory Impairments andNeurological Disorders, University of California, Irvine, CA, USA | [b] Department of Neurobiology and Behavior, University of California, Irvine, CA, USA
Correspondence: [*] Correspondence to: Alessandra C. Martini and Frank M. LaFerla, Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, USA. E-mails: ac.martini@uci.edu (A.C. Martini) laferla@uci.edu (F.M. LaFerla).
Abstract: Alzheimer’s disease (AD) impairs memory and causes significant cognitive deficits. The disease course is prolonged, with a poor prognosis, and thus exacts an enormous economic and social burden. Over the past two decades, genetically engineered mouse models have proven indispensable for understanding AD pathogenesis, as well as for discovering new therapeutic targets. Here we highlight significant studies from our laboratory that have helped advance the AD field by elucidating key pathogenic processes operative in AD and exploring a variety of aspects of the disease which may yield novel therapeutic strategies for combatting this burdensome disease.
Keywords: 3xTg-AD, amyloid-β, animal models, comorbidities, inflammation, stem cell therapy, synaptic loss, tau
DOI: 10.3233/JAD-179917
Journal: Journal of Alzheimer's Disease, vol. 64, no. s1, pp. S365-S378, 2018
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