{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T21:00:51Z","timestamp":1792270851742,"version":"4.4.0"},"reference-count":292,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2023,2,18]],"date-time":"2023-02-18T00:00:00Z","timestamp":1676678400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Antioxidants"],"abstract":"<jats:p>Neurodegenerative disorders constitute a substantial proportion of neurological diseases with significant public health importance. The pathophysiology of neurodegenerative diseases is characterized by a complex interplay of various general and disease-specific factors that lead to the end point of neuronal degeneration and loss, and the eventual clinical manifestations. Oxidative stress is the result of an imbalance between pro-oxidant species and antioxidant systems, characterized by an elevation in the levels of reactive oxygen and reactive nitrogen species, and a reduction in the levels of endogenous antioxidants. Recent studies have increasingly highlighted oxidative stress and associated mitochondrial dysfunction to be important players in the pathophysiologic processes involved in neurodegenerative conditions. In this article, we review the current knowledge of the general effects of oxidative stress on the central nervous system, the different specific routes by which oxidative stress influences the pathophysiologic processes involved in Alzheimer\u2019s disease, Parkinson\u2019s disease, Amyotrophic Lateral Sclerosis and Huntington\u2019s disease, and how oxidative stress may be therapeutically reversed\/mitigated in order to stall the pathological progression of these neurodegenerative disorders to bring about clinical benefits.<\/jats:p>","DOI":"10.3390\/antiox12020517","type":"journal-article","created":{"date-parts":[[2023,2,20]],"date-time":"2023-02-20T04:58:23Z","timestamp":1676869103000},"page":"517","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":653,"title":["Oxidative Stress and Antioxidants in Neurodegenerative Disorders"],"prefix":"10.3390","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4145-348X","authenticated-orcid":false,"given":"Edward O.","family":"Olufunmilayo","sequence":"first","affiliation":[{"name":"Laboratory of Molecular Neuroscience and Dementia, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia"},{"name":"Department of Medicine, University College Hospital, Queen Elizabeth Road, Oritamefa, Ibadan 5116, PMB, Nigeria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle B.","family":"Gerke-Duncan","sequence":"additional","affiliation":[{"name":"Education Innovation, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4447-0835","authenticated-orcid":false,"given":"R. M. Damian","family":"Holsinger","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Neuroscience and Dementia, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia"},{"name":"Neuroscience, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2023,2,18]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"24438","DOI":"10.3390\/ijms141224438","article-title":"Oxidative stress and neurodegenerative disorders","volume":"14","author":"Li","year":"2013","journal-title":"Int. J. Mol. 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