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Role of Oxidative Damage in Alzheimer's Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery
Buccellato FR, D'Anca M, Fenoglio C, Scarpini E, Galimberti D.. Antioxidants (Basel, Switzerland), 2021-08-26
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the discovery of biomarkers for early diagnosis, i.e., in subjects with mild cognitive impairment (MCI) or prodromal AD. The brain is exposed to oxidative stress as levels of reactive oxygen species (ROS) are increased, whereas cellular antioxidant defenses are decreased. Increased ROS levels can damage cellular structures or molecules, leading to protein, lipid, DNA, or RNA oxidation. Oxidative damage is involved in the molecular mechanisms which link the accumulation of amyloid-β and neurofibrillary tangles, containing hyperphosphorylated tau, to microglia response. In this scenario, microglia are thought to play a crucial role not only in the early events of AD pathogenesis but also in the progression of the disease. This review will focus on oxidative damage products as possible peripheral biomarkers in AD and in the preclinical phases of the disease. Particular attention will be paid to biological fluids such as blood, CSF, urine, and saliva, and potential future use of molecules contained in such body fluids for early differential diagnosis and monitoring the disease course. We will also review the role of oxidative damage and microglia in the pathogenesis of AD and, more broadly, in neurodegeneration.
Key findings
- Oxidative damage is involved in the molecular mechanisms which link the accumulation of amyloid-β and neurofibrillary tangles, containing hyperphosphorylated tau, to microglia response.
- In this scenario, microglia are thought to play a crucial role not only in the early events of AD pathogenesis but also in the progression of the disease.
- This review will focus on oxidative damage products as possible peripheral biomarkers in AD and in the preclinical phases of the disease.
- Particular attention will be paid to biological fluids such as blood, CSF, urine, and saliva, and potential future use of molecules contained in such body fluids for early differential diagnosis and monitoring the disease course.
- We will also review the role of oxidative damage and microglia in the pathogenesis of AD and, more broadly, in neurodegeneration.
Why it matters
This review discusses oxidative damage as a possible contributor to Alzheimer's disease mechanisms and as a source of peripheral biomarkers. It focuses on oxidative damage products in blood, cerebrospinal fluid, urine and saliva as possible tools for early diagnosis and monitoring, but reports no treatment or cure.
Study details
- Evidence strengthLow
How this study scored 49/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Antioxidants (Basel, Switzerland)) |
| Journal's citation record | 2 / 4 | Antioxidants: journal h-index 208 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2021 — within 6 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 179 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 25.6 citations a year over 7 year(s) since 2021 |
| Impact for its field and year | 4 / 6 | Cited 11.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 118 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Daniela Galimberti: h-index 94 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Milan: institution h-index 1,023 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34572985) |
| Free to read | 2 / 2 | Free to read |
| Total | 49 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Buccellato, F. R., D'Anca, M., Fenoglio, C., Scarpini, E., & Galimberti, D. (2021). Role of Oxidative Damage in Alzheimer's Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery. Antioxidants (Basel, Switzerland). https://doi.org/10.3390/antiox10091353
Vancouver
Buccellato FR, D'Anca M, Fenoglio C, Scarpini E, Galimberti D. Role of Oxidative Damage in Alzheimer's Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery. Antioxidants (Basel, Switzerland). 2021. doi:10.3390/antiox10091353. PMID: 34572985.
BibTeX
@article{buccellato2021-34572985,
author = {Buccellato, F. R. and D'Anca, M. and Fenoglio, C. and Scarpini, E. and Galimberti, D.},
title = {{Role of Oxidative Damage in Alzheimer's Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery}},
journal = {Antioxidants (Basel, Switzerland)},
year = {2021},
doi = {10.3390/antiox10091353},
pmid = {34572985},
url = {https://doi.org/10.3390/antiox10091353}
}
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