{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T16:39:19Z","timestamp":1789403959724,"version":"build-2803163510"},"reference-count":287,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2018,10,16]],"date-time":"2018-10-16T00:00:00Z","timestamp":1539648000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Cerebrovascular and neurodegenerative disorders affect one billion people around the world and result from a combination of genomic, epigenomic, metabolic, and environmental factors. Diagnosis at late stages of disease progression, limited knowledge of gene biomarkers and molecular mechanisms of the pathology, and conventional compounds based on symptomatic rather than mechanistic features, determine the lack of success of current treatments, including current FDA-approved conventional drugs. The epigenetic approach opens new avenues for the detection of early presymptomatic pathological events that would allow the implementation of novel strategies in order to stop or delay the pathological process. The reversibility and potential restoring of epigenetic aberrations along with their potential use as targets for pharmacological and dietary interventions sited the use of epidrugs as potential novel candidates for successful treatments of multifactorial disorders involving neurodegeneration. This manuscript includes a description of the most relevant epigenetic mechanisms involved in the most prevalent neurodegenerative disorders worldwide, as well as the main potential epigenetic-based compounds under investigation for treatment of those disorders and their limitations.<\/jats:p>","DOI":"10.3390\/ijms19103199","type":"journal-article","created":{"date-parts":[[2018,10,16]],"date-time":"2018-10-16T11:07:51Z","timestamp":1539688071000},"page":"3199","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":63,"title":["Pharmacoepigenomic Interventions as Novel Potential Treatments for Alzheimer\u2019s and Parkinson\u2019s Diseases"],"prefix":"10.3390","volume":"19","author":[{"given":"Oscar","family":"Teijido","sequence":"first","affiliation":[{"name":"EuroEspes Biomedical Research Center, Institute of Medical Science and Genomic Medicine, 15165 La Coru\u00f1a, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0554-4037","authenticated-orcid":false,"given":"Ram\u00f3n","family":"Cacabelos","sequence":"additional","affiliation":[{"name":"EuroEspes Biomedical Research Center, Institute of Medical Science and Genomic Medicine, 15165 La Coru\u00f1a, Spain"},{"name":"Chair of Genomic Medicine, Continental University Medical School, Huancayo 12000, Peru"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2018,10,16]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"1361","DOI":"10.1016\/j.cell.2006.10.043","article-title":"Structural basis for the methylation statespecific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair","volume":"127","author":"Botuyan","year":"2006","journal-title":"Cell"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1059","DOI":"10.1517\/17460441.2014.930124","article-title":"Epigenetic drug discovery for Alzheimer\u2019s disease","volume":"9","author":"Cacabelos","year":"2014","journal-title":"Expert Opin. 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