The DOI matches its Crossref record; 185 of the 188 references it cites were found in a registry or an index.
Neuroprotective strategies involving ROS in Alzheimer disease
Open accessAbstract
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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“Oxidative stress markers increase even in the preclinical phase and during MCI, while antioxidant therapies in animal models have been shown to delay the disease course and improve cognitive functions [122, 123].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [123]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“In contrast, in advanced AD—characterized by widespread neuronal damage and complex pathological remodeling—the effectiveness of antioxidant therapy is significantly reduced. Numerous unsuccessful clinical trials have reported minimal cognitive improvements in patients at advanced disease stages [123–125].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [123]
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“Scientific evidence clearly indicates that targeting ROS and oxidative stress is more effective during the early stages of AD than in advanced stages.”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [123]
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“In summary, ROS-targeting strategies exhibit the greatest efficacy in early AD, before irreversible neuronal damage occurs [122, 123].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [123]
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1 retracted
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Oxidative Damage Is the Earliest Event in Alzheimer Disease
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Research works printed but not linked: 1
- 2010, Acetyl-L-carnitine, Monogr. Altern. Med. Rev., 15, 76
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Bioinorganic Chemistry of Alzheimer’s Disease
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Metadata
- Authors
- Dumont, M., & Beal, M. F.
- Affiliations
- Weill Cornell Medicine (US)
- Corresponding author
- Dumont, Magali
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 51
- Issue
- 5
- Pages
- 1014-1026
- ISSN
- 0891-5849 (ISSN-L)
- 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
- 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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