Journal
CURRENT GENE THERAPY
Volume 18, Issue 3, Pages 143-153Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1566523218666180430121323
Keywords
miR-7; Parkinson's disease; Neurodegeneration; RNAi; MicroRNA; Synuclein; Lewy body; Synucleinopathy
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Funding
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - CAPES
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - CNPq
- Fundacao de Apoio a Pesquisa do Distrito Federal - FAP-DF
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The present review examines whether the microRNA 7 (miR-7) holds potential for slowing Parkinson's disease (PD) progression. First, the accurate expression of miR-7 allows for normal development, physiology, and neurogenesis in the central nervous system, also keeping alpha-synuclein (alpha-Syn) at the physiological level. Second, patients with PD and parkinsonian MPTP-induced animals exhibit a significant decrease of miR-7 in brain areas associated with dopaminergic neurodegeneration. Depletion of miR-7 in the substantia nigra of clinical samples is related to alpha-Syn accumulation, loss of dopaminergic cells, and reduction of dopamine in the striatum. Therefore, the goal of a miR-7-replacement therapy is to downregulate alpha-Syn and other PD-related genes, achieving multi-target benefits regarding oxidative stress, mitochondrial health, cell glycolysis, apoptosis, and inhibition of inflammasome activation. While a disease-modifying drug is a major unmet need for the clinical management of PD, an miR-7-replacement therapy presents a striking potential against critical mechanisms of neuropathology. Such innovative treatment would reduce alpha-Syn accumulation in the Lewy bodies and preserve remaining neurons yet viable at the time of diagnosis, thus slowing disease progression from the early phase of PD characterized by a relatively mild motor impairment to an advanced and more disabling stage.
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