Mitochondria in Neuroplasticity and Neurological Disorders

Mark P. Mattson, Marc Gleichmann, Aiwu Cheng

Research output: Contribution to journalArticle

Abstract

Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function. Mitochondria are highly dynamic organelles that divide, fuse, and move purposefully within axons and dendrites. Major functions of mitochondria in neurons include the regulation of Ca2+ and redox signaling, developmental and synaptic plasticity, and the arbitration of cell survival and death. The importance of mitochondria in neurons is evident in the neurological phenotypes in rare diseases caused by mutations in mitochondrial genes. Mitochondria-mediated oxidative stress, perturbed Ca2+ homeostasis, and apoptosis may also contribute to the pathogenesis of prominent neurological diseases including Alzheimer's, Parkinson's, and Huntington's diseases; stroke; amyotrophic lateral sclerosis; and psychiatric disorders. Advances in understanding the molecular and cell biology of mitochondria are leading to novel approaches for the prevention and treatment of neurological disorders.

Original languageEnglish (US)
Pages (from-to)748-766
Number of pages19
JournalNeuron
Volume60
Issue number5
DOIs
StatePublished - Dec 10 2008
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Mattson, M. P., Gleichmann, M., & Cheng, A. (2008). Mitochondria in Neuroplasticity and Neurological Disorders. Neuron, 60(5), 748-766. https://doi.org/10.1016/j.neuron.2008.10.010