Cited by 1,081Mitochondrial Function and PathologyAutophagy in Disease and TherapyPharmacological Receptor Mechanisms and Effects

Mitochondria in neuroplasticity and neurological disorders

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Mattson, Mark P., Gleichmann, Marc, Cheng, Aiwu·2008·Neuron

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 Ca(2+) 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 Ca(2+) 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.

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Crossref · 10.1016/j.neuron.2008.10.010

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210 of 210 references verified0 citation errors · 0 not checkable

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  • In neurons, mitochondria generate ATP through oxidative phosphorylation in order to sustain synaptic transmission and cell maintenance/repair.

    “In neurons, mitochondria generate ATP through oxidative phosphorylation in order to sustain synaptic transmission and cell maintenance/repair.73,75”

    From Uncovering the signatures of aging and senescence in the human dorsolateral prefrontal cortex (2026) · cites this paper as [75]

    The Structure and Regulatory Systems of Mitochondria section describes ATP production by the electron transport chain, and Mitochondria in Synaptic Plasticity links mitochondrial ATP to synaptic function. The Abstract says this ATP is essential for neuronal survival, which supports cell maintenance, but the passages do not establish a role in cell repair. Page numbers are unavailable in our copy. (LLM, conf=0.84)

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  • Mitochondrial dysfunction is a known hallmark of the aging brain and neurodegenerative disorders.

    “Mitochondrial dysfunction is a known hallmark of the aging brain73,74 and neurodegenerative disorders.75,76,77”
  • Mitochondria generate ATP for neuronal activities including neurotransmission and Ca2+ homeostasis and provide signals regulating nuclear-mitochondrial communication and neuronal survival/death.

    “Mitochondria generate ATP to support neuronal activities including neurotransmission and Ca2+ homeostasis and are a source of signals that regulate nuclear-mitochondrial communication and even the arbitration of neuronal survival and death (Mattson et al., 2008).”

    From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Mattson et al., 2008

  • Mitochondria from animal and post-mortem human brain tissues show age-dependent increases in functional heterogeneity, oxidative damage, reduced ETC function, disrupted membrane potential, impaired Ca2+ handling, and/or accumulation of dysfunctional mitochondria.

    “Mitochondria isolated from animal and post-mortem human brain tissues show an age-dependent rise in mitochondrial functional heterogeneity, increased oxidative damage, reduced function of the ETC, disrupted membrane potential, impaired Ca2+ handling, and/or an accumulation of dysfunctional mitochondria (Lin and Beal, 2006; Mattson et al., 2008; Sorrentino et al., 2017).”

    From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Mattson et al., 2008

  • On the basis of evidence from post-mortem brain tissues from Alzheimer's disease patients and different AD mouse models, damaged mitochondria and increased oxidative stress are common features of Alzheimer's disease.

    “On the basis of evidence from post-mortem brain tissues from AD patients as well as different AD mouse models, damaged mitochondria and increased oxidative stress are common features of AD (Lin and Beal, 2006; Mattson et al., 2008).”

    From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Mattson et al., 2008

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Authors
Mattson, M. P., Gleichmann, M., & Cheng, A.
Affiliations
National Institute on Aging (US)
Corresponding author
Mattson, Mark P.
Venue
Neuron
Publisher
Elsevier BV
Published
2008-12
Volume
60
Issue
5
Pages
748-766
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2010179451
Cited by
1,081
References
210
Citations by year
2026: 57 · 2025: 59 · 2024: 58 · 2023: 67 · 2022: 74 · 2021: 89 · 2020: 83 · 2019: 62 · 2018: 61 · 2017: 69 · 2016: 65 · 2015: 50 · 2014: 44 · 2013: 47 · 2012: 65
FWCI
3.32
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
Keywords
mitochondria, neuroplasticity, neurological disorders, mitochondrial dynamics, mitochondrial fission and fusion, calcium homeostasis, redox signaling, synaptic plasticity, neuronal excitability, mitochondrial DNA mutations, oxidative stress, apoptosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke, amyotrophic lateral sclerosis, mental illness
MeSH terms
Animals, Humans, Mitochondria, Models, Biological, Nervous System Diseases, Neuronal Plasticity, Mitochondrial Proteins, Electron Transport Complex I

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