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Updated: Jan 23, 2026

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Characterization of pH-Dependent Reversible Self-Assembly of Amyloid Beta 1-40-Coated Gold Colloids
Published on: March 21, 2025
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Amyloid beta peptide, 4-hydroxynonenal and apoptosis
Mark A Lovell1, William R Markesbery
1Department of Chemistry, University of Kentucky, Lexington, KY 40536, USA. malove2@uky.edu
Current Alzheimer Research
|October 5, 2006
Summary
Oxidative stress and its toxic by-products contribute to neuron degeneration in Alzheimer's disease (AD). This review examines evidence for oxidative stress-mediated apoptosis in in vitro AD models.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Oxidative stress is implicated in neurodegenerative disorders like Alzheimer's disease (AD).
- Key contributors include amyloid beta peptide, iron/hydrogen peroxide, and lipid peroxidation by-products (4-hydroxy-2-nonenal, acrolein).
Purpose of the Study:
- To review evidence supporting the role of oxidative stress in AD pathogenesis.
- To focus on oxidative stress-mediated apoptosis in in vitro models.
Main Methods:
- Literature review of in vitro studies on neurodegeneration.
- Analysis of mechanisms linking oxidative stress/damage to apoptosis in AD models.
Main Results:
- Evidence suggests oxidative stress and specific toxic by-products induce apoptosis in neuronal cells.
- In vitro models demonstrate the link between oxidative damage and programmed cell death.
Conclusions:
- Oxidative stress-mediated apoptosis is a significant factor in AD neurodegeneration.
- In vitro studies provide valuable insights into these mechanisms.
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