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Article type: Review Article
Authors: Di Meco, Antonio | Praticò, Domenico*
Affiliations: Department of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA
Correspondence: [*] Correspondence to: Domenico Praticò, MD, 947, Medical Education and Research Building, 3500 North Broad Street, Philadelphia, PA 19140, USA. Tel.: +1 215 707 9380; Fax: +1 215 707 9890; E-Mail: praticod@temple.edu.
Abstract: Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. With increasing longevity and the absence of a cure, AD has become not only a major health problem but also a heavy social and economic burden worldwide. Given this public health challenge, and that the current approved therapy for AD is limited to symptomatic treatment (i.e., cholinesterase inhibitors and NMDA receptor antagonists), exploration of new molecular pathways as novel therapeutic targets remains an attractive option for disease modifying drug development. microRNAs (miRNAs) are short non-coding RNA that control gene expression at the post-translational level by inhibiting translation of specific mRNAs or degrading them. Dysregulation of several miRNAs has been described in AD brains. Interestingly, their molecular targets are pathways that are well-established functional players in the onset and development of AD pathogenesis. Today several molecular tools have been developed to modulate miRNA levels in vitro and in vivo. These scientific advancements are affording us for the first time with the real possibility of targeting in vivo these dysregulated miRNAs as a novel therapeutic approach against AD.
Keywords: Alzheimer’s disease, amyloid-beta, microRNAs, neuroinflammation, tau, therapeutic target
DOI: 10.3233/JAD-160203
Journal: Journal of Alzheimer's Disease, vol. 53, no. 2, pp. 367-372, 2016
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