Mitochondria in Neuroplasticity and Neurological Disorders

By Mark P. Mattson, M. Gleichmann, A. Cheng. Neuron, 2008

1,037 citations recorded by the source corpus.

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. An 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, ALS 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.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/81f5e0bff8d107412a090a284f1263f6954a1412

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Citations in the corpus

Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Over the past decade considerable advances have been made in the understanding of the nature of the dose response, especially in the low-dose zone (88, 116, 204, 280, 291, 292, 398).”
Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicity (2011, background): “Mitochondria: paradoxical organelles Mitochondria play a pivotal role in cell survival and death by regulating both energy metabolism and apoptotic pathways (Figure 1); they contribute to many cellular functions, including intracellular calcium homeostasis, the alteration of the cellular reduction-o”
Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States (2018, background): “…et al., 2017), impaired adaptive stress response signaling (Stranahan andMattson, 2012), dysregulated neuronal Ca2+ homeostasis (Bezprozvanny and Mattson, 2008; Stutzmann and Mattson, 2011), impaired energy metabolism (Dauncey, 2014), neuroinflammation (Heppner et al., 2015), and stem cell…”
Cannabinoid Receptors and the Endocannabinoid System: Signaling and Function in the Central Nervous System (2018, background): “These lines of evidence highlight the direct association between mitochondrial CB1R and proper functioning of mitochondria, which has been suggested to participate in many pathological conditions [84,85].”
Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+ transfer to mitochondria. (2010, neutral): “…including cancer (Vander Heiden et al., 2009), insufficient nutrient availability, ischemia, injury and exposure to metabolic inhibitors (Huttemann et al., 2008), neurodegenerative (Mattson et al., 2008) and cardiovascular (Gustafsson and Gottlieb, 2008) diseases, and aging (Balaban et al., 2005).”
Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “In support of a “vicious cycle” hypothesis, Aβ and pTau can adversely affect mitochondrial function and integrity in vitro and in vivo [10, 16].”
The dynamin-related GTPase Drp1 is required for embryonic and brain development in mice (2009, background): “Normal mitochondrial dynamics are critical for human health and disease (Knott and Bossy-Wetzel, 2008; Mattson et al., 2008).”