Positive Feedback Relationship between Lipid Peroxidation and Amyloidogenesis Offers Insights into the Pathogenesis of Alzheimer's Disease

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  • Author(s): Paddock, Brie; Davenport, Caty
  • Language:
    English
  • Source:
    HAPS Educator. Dec 2017 21(3):20-24.
  • Publication Date:
    2017
  • Document Type:
    Journal Articles
    Reports - Evaluative
  • Additional Information
    • Availability:
      Human Anatomy and Physiology Society. PO Box 2945, LeGrange, GA 30421. e-mail: [email protected]; Web site: https://www.hapsweb.org/page/hapsed_home
    • Peer Reviewed:
      Y
    • Source:
      6
    • Subject Terms:
      Alzheimers Disease; Physiology; Anatomy; Neurology; Brain
    • ISSN:
      2473-3806
    • Abstract:
      Alzheimer's disease is a progressive neurodegenerative disorder characterized by amyloid plaques, synapse dysfunction, and memory loss. The production and accumulation of A[beta] peptides, a major component of the amyloid plaques, is sensitive to many genetic and environmental factors. Recently, research has focused on the role of oxidative stress in initiating or exacerbating the neurodegeneration associated with A[beta] production. Lipid peroxidation, a type of oxidative stress that results in damaging cellular products such as 4-hydroxynonenal (HNE), has been demonstrated to increase the concentration of A[beta] peptides through several mechanisms. In addition to their association with memory loss and synapse dysfunction, these A[beta] peptides cause lipid peroxidation. This positive feedback relationship between lipid peroxidation and A[beta] peptides may be the causative sequence of events initiating the pathogenic cascade of AD. This article examines the relationship between lipid peroxidation and amyloidogenesis in order to determine the sequence of events leading to A[beta]-plaque deposition and potential treatments with antioxidants targeting lipid peroxidation and its products.
    • Abstract:
      As Provided
    • Publication Date:
      2019
    • Accession Number:
      EJ1228002