The role of oxidative stress in neurodegenerative diseases and potential antioxidant therapies

Sienes Bailo, P. ; Llorente Martín, E. ; Calmarza, P. ; Montolio Breva, S. ; Bravo Gómez, A. ; Pozo Giráldez, A. ; Sánchez-Pascuala Callau, J. J. ; Vaquer Santamaría, J. M. ; Dayaldasani Khialani, A. ; Cerdá Micó, C. ; Camps Andreu, J. ; Sáez Tormo, G. ; Fort Gallifa, I.

Resumen: Objectives: The central nervous system (CNS) is essential for homeostasis and controls the physiological functions of the body. However, the biochemical characteristics of the CNS make it especially vulnerable to oxidative damage (OS). This phenomenon compromises correct CNS functioning, leading to neurodegeneration and neuronal death. Contents: OS plays a crucial role in the physiopathology of neurodegenerative diseases. It is involved in multiple mechanisms of nucleic acid, protein, and lipid oxidation, thereby contributing to progressive brain damage. These mechanisms include mitochondrial dysfunction; excessive production of reactive oxygen and nitrogen species; deficiency of antioxidant defenses; protein oligomerization; cytokine production and inflammatory response; blood–brain barrier abnormalities; and proteasome dysfunction. All these dysfunctions are involved in the pathogenesis of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, or amyotrophic lateral sclerosis. Summary and outlook: A curative treatment is currently not available. Research is focused on the search for therapies that reduce oxidative damage and delay disease progression. In the recent years, researchers have focused their attention on the effects of antioxidant therapies.

Idioma: Inglés

DOI: 10.1515/almed-2022-0111

Año: 2022

Publicado en: Advances in laboratory medicine 3, 4 (2022), 342-350
ISSN: 2628-491X

Factor impacto CITESCORE: 0.7 - Social Sciences (Q3) - Health Professions (Q4) - Medicine (Q4)

Factor impacto SCIMAGO: 0.199 - Medical Laboratory Technology (Q3) - Medicine (miscellaneous) (Q4) - Education (Q4)

Tipo y forma: Artículo (Versión definitiva)