| Literature DB >> 26899010 |
Michael H Irwin1, Walter H Moos2,3, Douglas V Faller4, Kosta Steliou4,5, Carl A Pinkert1,6.
Abstract
Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016.Entities:
Keywords: Alzheimer; PMX-500; PMX-550; Parkinson; antioxidant; butyrate; carnitine; epigenetic; histone deacetylase; histone deacetylase inhibitors; lipoic acid; mitochondrial dysfunction; neurodegeneration; post-traumatic stress disorders; reactive oxygen species
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Year: 2016 PMID: 26899010 DOI: 10.1002/ddr.21294
Source DB: PubMed Journal: Drug Dev Res ISSN: 0272-4391 Impact factor: 4.360