Cited by 407Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroprotection in Cerebral Ischemia

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Neuroprotective strategies involving ROS in Alzheimer disease

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Dumont, Magali, Beal, M. Flint·2011·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2010.11.026PMC PMC3070183

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Abstract

Alzheimer disease (AD) is a neurodegenerative disorder in which oxidative stress is a key hallmark. It occurs early in disease pathogenesis and can exacerbate its progression. Several causes of oxidative stress have been determined over the years. First, mitochondria play an important role in the generation and accumulation of free radicals. In addition to mitochondria, inflammation can also induce oxidative damage, especially via microglia, and microglia are also important for Aβ clearance. In AD, both mitochondrial function and inflammatory response are affected, leading to increased ROS formation and oxidative damage to lipid, proteins, and nucleic acids. Some other sources have also been identified. From these findings, various neuroprotective strategies against ROS-mediated damages have been elaborated in AD research. This review recapitulates some of the major strategies used to prevent oxidative stress and disease progression. Outcomes from in vitro and in vivo studies using models of AD are encouraging. However, only a few clinical trials have provided positive results in terms of slowing down cognitive decline. Nonetheless, there is still hope for improved compounds that would better target pathways implicated in ROS production. In fact, facilitating the endogenous antioxidant system by modulating transcription has great promise for AD therapy.

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Authors: Dumont, M., & Beal, M. F.
Affiliations: Weill Cornell Medicine (US)
Corresponding author: Dumont, Magali
ORCID: Dumont, Magali
Beal, M. Flint
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2011-09
Volume: 51
Issue: 5
Pages: 1014-1026
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2010.11.026
PMC: PMC3070183
OpenAlex: W2080084871
Cited by: 402
References: 188
Citations by year: 2026: 12 · 2025: 19 · 2024: 21 · 2023: 20 · 2022: 21 · 2021: 22 · 2020: 26 · 2019: 28 · 2018: 19 · 2017: 36 · 2016: 28 · 2015: 29 · 2014: 36 · 2013: 34 · 2012: 34
FWCI: 2.76
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute on Aging (R01AG20729, R01AG020729, P01AG014930, P01-AG14930)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords: Alzheimer's disease, reactive oxygen species, oxidative stress, neuroprotection, mitochondria, microglia, neuroinflammation, amyloid-beta clearance, antioxidant defense, transcriptional regulation, neurodegeneration, cognitive decline
MeSH terms: Alzheimer Disease, Animals, Antioxidants, Clinical Trials as Topic, Disease Models, Animal, Humans, Inflammation, Mitochondria, Oxidation-Reduction, Reactive Oxygen Species, Microglia, Oxidative Stress, Disease Progression, Neuroprotective Agents, Molecular Targeted Therapy

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