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NARRATIVE REVIEW
Year : 2021  |  Volume : 8  |  Issue : 2  |  Page : 171-186

Deciphering and manipulating the epigenome for the treatment of Parkinson’s and Alzheimer’s disease


Department of Public Health and Infectious Diseases, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy

Correspondence Address:
Dr. Chidiebere Emmanuel Okechukwu
Department of Public Health and Infectious Diseases, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome.
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mgmj.mgmj_90_20

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Precision medicine intends to tailor medical practice with a focus on the individual, built on the utilization of genetic tests, the identification of biomarkers, and the development of targeted medicines, and this can be achieved by having a complex knowledge of epigenetic mechanisms. Parkinson’s disease (PD) is an age-linked neurodegenerative disease that affects majorly individuals above 65; there is a growing indication that epigenetic disruption and dysregulation in the expression of micro-ribonucleic acids (miRNAs) arise in PD. Genome-wide association studies discovered a straightforward consequence of the methylation status of α-synuclein in the pathogenesis of PD. Alzheimer’s disease (AD) is a form of neurodegenerative disease, epitomized by memory loss. The dysregulation of non-coding RNAs and epigenetic aberrations have been identified in AD. This narrative review aimed to elaborate on the potential epigenomic treatments for PD and AD. About 199 scientific articles written in English, which reported on novel epigenomic-based treatment for PD and AD, were selected for this review from the PubMed database. Full articles and relevant data were extracted. Treatments targeting DNA methylation or miRNAs appear to show promising outcomes for PD and AD. Moreover, the clustered regularly interspaced short palindromic repeats and associated protein 9 is a potential genome editing tool for deciphering and manipulating the epigenome for the treatment of PD and AD.


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