Exocytosis, Mitochondrial Injury and Oxidative Stress in Neurodegenerative Diseases

Mark P. Zanin, Damien J. Keating

    Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

    1 Citation (Scopus)

    Abstract

    Common features seen in the early stages of many neurodegenerative diseases include increases in oxidative stress and mitochondrial dysfunction, ultimately leading to defects in cellular energy production. These changes particularly affect cells that are highly active, such as neurons. As such, reduced synaptic transmission is a common early feature associated with neurodegenerative diseases, such as Parkinson s disease, Alzheimer s disease, Huntington s disease and Amyotrophic Lateral Sclerosis. Many genes associated with neurodegenerative diseases are now known to regulate either mitochondrial function, redox state or the exocytosis of neurotransmitters. Mitochondria are a significant source of cellular ATP and reactive oxygen species and are prevalent in synapses at areas of exocytosis. Therefore, it follows that reductions in mitochondrial function and/or increases in oxidative stress will impact on neurotransmission.

    Original languageEnglish
    Title of host publicationOxidative Neural Injury
    EditorsSigrid C. Veasey
    Place of PublicationUnited States
    PublisherHumana Press
    Pages65-81
    Number of pages17
    ISBN (Electronic)978-1-60327-342-8
    ISBN (Print)978-1-60327-341-1, 978-1-61737-892-8
    DOIs
    Publication statusPublished - 22 Jun 2009

    Publication series

    NameContemporary Clinical Neuroscience
    PublisherSpringer
    ISSN (Print)2627-535X
    ISSN (Electronic)2627-5341

    Keywords

    • Alzheimer s disease
    • Amyotrophic lateral sclerosis
    • Exocytosis
    • Huntington s disease
    • Long-term potentiation
    • Mitochondria
    • Neurotransmission
    • Oxidative stress
    • Parkinson s disease
    • SNARE proteins
    • Synaptic transmission
    • β-amyloid

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