Oxidation of Aβ and Plaque Biogenesis in Alzheimer's Disease and Down Syndrome
Open accessAbstract
The processes involved with beta-amyloid (Abeta) degradation and clearance in human brain are not well understood. We hypothesized that the distribution of oxidatively modified Abeta, as determined by an affinity-purified antibody in the entorhinal and frontal cortices of Alzheimer's disease (AD), Down syndrome (DS), nondemented elderly control cases, and canine brain, would provide insight into the mechanisms of Abeta accumulation. Based upon plaque counts, oxidized Abeta was present within 46-48% of diffuse and primitive plaques and 98% of cored plaques. Dense punctate deposits of oxidized Abeta were distributed throughout the neuropil in AD and DS brains but were also present within controls with mild neuropathology and isolated cognitive impairments. Confocal studies indicate that punctate oxidized Abeta deposits were within activated microglia. Oxidatively modified Abeta may reflect the efforts of microglial cells to take up and degrade Abeta. Oxidative modification of Abeta may be an early event in Abeta pathogenesis and may be important for plaque biogenesis.
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Analysis confirmed occurrence of glycation end products and process of glycoxidation triggered very early in prenatal life.
“The analysis confirmed the occurrence of glycation end products and that the process of glycoxidation is triggered very early in prenatal life (Head et al. 2001).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Head et al. 2001
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References 77 · Cited by 75
- Authors
- Head, E., Garzon-Rodriguez, W., Johnson, J. K., Lott, I. T., Cotman, C. W., & Glabe, C.
- Affiliations
- University of California, Irvine (US)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2001-10
- Volume
- 8
- Issue
- 5
- Pages
- 792-806
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2006173276
- Cited by
- 75
- References
- 77
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 5 · 2019: 1 · 2017: 2 · 2016: 1 · 2015: 6 · 2014: 2 · 2013: 1 · 2012: 3
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (AG00538, AG12694, AG16573)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, Down syndrome, amyloid plaques, microglia, amyloid clearance, entorhinal cortex, frontal cortex, oxidative modification, diffuse plaques
- MeSH terms
- Alzheimer Disease, Brain, Down Syndrome, HLA-DR Antigens, Humans, Oxidation-Reduction, Amyloid beta-Peptides, Microglia, Microscopy, Confocal, Plaque, Amyloid
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