{"title":"Free radicals in Alzheimer's disease: from pathophysiology to clinical trial results.","authors":"José Viña, Consuelo Borrás, Cristina Mas-Bargues","doi":"10.1016/j.freeradbiomed.2024.09.051","DOIUrl":null,"url":null,"abstract":"<p><p>In this review, we examine the role of oxidative stress in the pathophysiology of Alzheimer's Disease (AD). Amyloid-beta (Aβ) induces damage not only extracellularly but also within the intracellular environment. Mitochondria, a principal source of free radicals, are closely associated with Aβ, as it binds to heme, thereby disrupting the normal electron flow in the respiratory chain. At the turn of the century, it was hypothesized that the majority, if not all, pathological events in AD are linked to free radical damage. Notably, free radicals also possess signaling capabilities that contribute to the disease's progression. A substantial body of evidence suggests that radical signaling is implicated in the relationship between amyloid-β and tau hyperphosphorylation. Antioxidant therapy represents a potential strategy to delay the progression from cognitive impairment to overt dementia. Enhancing endogenous antioxidant defenses, for instance, through polyphenol supplementation, offers a promising approach to partially prevent dementia onset, particularly in at-risk populations. Understanding the redox-related pathophysiology of AD opens new avenues for prevention and treatment, providing a source of hope in the fight against Alzheimer's Disease.</p>","PeriodicalId":12407,"journal":{"name":"Free Radical Biology and Medicine","volume":null,"pages":null},"PeriodicalIF":7.1000,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Free Radical Biology and Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.freeradbiomed.2024.09.051","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
In this review, we examine the role of oxidative stress in the pathophysiology of Alzheimer's Disease (AD). Amyloid-beta (Aβ) induces damage not only extracellularly but also within the intracellular environment. Mitochondria, a principal source of free radicals, are closely associated with Aβ, as it binds to heme, thereby disrupting the normal electron flow in the respiratory chain. At the turn of the century, it was hypothesized that the majority, if not all, pathological events in AD are linked to free radical damage. Notably, free radicals also possess signaling capabilities that contribute to the disease's progression. A substantial body of evidence suggests that radical signaling is implicated in the relationship between amyloid-β and tau hyperphosphorylation. Antioxidant therapy represents a potential strategy to delay the progression from cognitive impairment to overt dementia. Enhancing endogenous antioxidant defenses, for instance, through polyphenol supplementation, offers a promising approach to partially prevent dementia onset, particularly in at-risk populations. Understanding the redox-related pathophysiology of AD opens new avenues for prevention and treatment, providing a source of hope in the fight against Alzheimer's Disease.
期刊介绍:
Free Radical Biology and Medicine is a leading journal in the field of redox biology, which is the study of the role of reactive oxygen species (ROS) and other oxidizing agents in biological systems. The journal serves as a premier forum for publishing innovative and groundbreaking research that explores the redox biology of health and disease, covering a wide range of topics and disciplines. Free Radical Biology and Medicine also commissions Special Issues that highlight recent advances in both basic and clinical research, with a particular emphasis on the mechanisms underlying altered metabolism and redox signaling. These Special Issues aim to provide a focused platform for the latest research in the field, fostering collaboration and knowledge exchange among researchers and clinicians.