ArticleNeuroscience letters2024
Methionine oxidation of clusterin in Alzheimer's disease and its effect on clusterin's binding to beta-amyloid.
Article in Neuroscience letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Increased Blood Plasma Levels of Methionine-Oxidized Clusterin Correlate with a Shift from Normal to Mild Cognitive Impairment and Alzheimer's Disease Stages.Antioxidants (Basel, Switzerland) · 2026Article
- 3,4-Dihydroxybenzaldehyde Exerts Anti-Alzheimer's Effects by Inhibiting Aβ Protofibril Assembly and Activating Antioxidant Defense Mechanisms.International journal of molecular sciences · 2026Article
- Mapping cerebrospinal fluid biomarkers to dementia risk through Mendelian randomization.Medicine · 2025Article
- Exfoliation syndrome genetics in the era of post-GWAS.Vision research · 2025Review
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4 authors.
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Abstract
Clusterin is a secreted glycoprotein that participates in multiple physiological processes through its chaperon function. In Alzheimer's disease, the brain functions under an increased oxidative stress condition that causes an elevation of protein oxidation, resulting in enhanced pathology. Accordingly, it is important to determine the type of human brain cells that are mostly prone to methionine oxidation in Alzheimer's disease and specifically monitoring the methionine-oxidation levels of clusterin in human and mice brains and its effect on clusterin's function. We analyzed the level of methionine sulfoxide (MetO)-clusterin in these brains, using a combination of immunoprecipitation and Western-blott analyses. Also, we determine the effect of methionine oxidation on clusterin ability to bind beta-amyloid, in vitro, using calorimetric assay. Our results show that human neurons and astrocytes of Alzheimer's disease brains are mostly affected by methionine oxidation. Moreover, MetO-clusterin levels are elevated in postmortem Alzheimer's disease human and mouse brains in comparison to controls. Finally, oxidation of methionine residues of purified clusterin reduced its binding efficiency to beta-amyloid. In conclusion, we suggest that methionine oxidation of brain-clusterin is enhanced in Alzheimer's disease and that this oxidation compromises its chaperon function, leading to exacerbation of beta-amyloid's toxicity in Alzheimer's disease.
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