Cited by 95Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyAutophagy in Disease and Therapy

Mitochondrial dysfunction in astrocytes: A role in Parkinson’s disease?

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Bantle, Collin M., Hirst, Warren D., Weihofen, Andreas, Shlevkov, Evgeny·2021·Frontiers in Cell and Developmental Biology

Abstract

Mitochondrial dysfunction is a hallmark of Parkinson’s disease (PD). Astrocytes are the most abundant glial cell type in the brain and are thought to play a pivotal role in the progression of PD. Emerging evidence suggests that many astrocytic functions, including glutamate metabolism, Ca 2+ signaling, fatty acid metabolism, antioxidant production, and inflammation are dependent on healthy mitochondria. Here, we review how mitochondrial dysfunction impacts astrocytes, highlighting translational gaps and opening new questions for therapeutic development.

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Crossref · 10.3389/fcell.2020.608026

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  • These changes contribute to mitochondrial dysfunction, synaptic loss, and neuronal degeneration, all of which are hallmark features of age-related neurodegenerative diseases such as Alzheimer's and Parkinson's disease.

    “These changes contribute to mitochondrial dysfunction, synaptic loss, and neuronal degeneration, all of which are hallmark features of age-related neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease (Joshi et al., 2019; Bantle et al., 2020).”

    From Aging promotes an increase in mitochondrial fragmentation in astrocytes (2024) · cites this paper as Bantle et al., 2020

    The Introduction identifies dopaminergic neuronal degeneration as a pathological hallmark of Parkinson’s disease and implicates mitochondrial dysfunction in its pathogenesis. It does not identify synaptic loss as a hallmark or establish the same set of features for Alzheimer’s disease, which it mentions only for comparison. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • With advancing age, alterations in mitochondrial dynamics occur in the brain, characterized by increased mitochondrial fragmentation and impaired mitochondrial fusion.

    “With advancing age, alterations in mitochondrial dynamics occur in the brain, characterized by increased mitochondrial fragmentation and impaired mitochondrial fusion.”

    From Aging promotes an increase in mitochondrial fragmentation in astrocytes (2024) · cites this paper as Bantle et al., 2020

    The Introduction (page unavailable) says mitochondrial dysfunction is a hallmark of aging. The section on astrocyte inflammatory activation discusses possible mitochondrial fragmentation from PINK1 or Parkin mutations, not from aging; our copy does not establish age-related fragmentation or impaired fusion in the brain. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • The specific role of substantia nigra pars compacta astrocytic mitochondria in contributing to neurodegeneration is a relatively unexplored but active area of investigation.

    “the specific role of SNc astrocytic mitochondria in contributing to neurodegeneration is a relatively unexplored, but active area of investigation”

    From Mitochondrial DNA Damage in Substantia Nigra Pars Compacta Astrocytes Exacerbates Dopaminergic Neuron Loss in a 6-Hydroxydopamine Mouse Model of Parkinsonism (2026) · cites this paper as Bantle et al. 2020

    The “Astrocyte Mitochondrial Function and Dysfunction in PD” section (page unavailable) calls astrocytic mitochondrial dysfunction an emerging field and suggests it may contribute to PD progression. However, “Astrocytes and Therapeutic Considerations in PD” (page unavailable) focuses on mitochondria in striatal astrocytes supporting SNpc axons; it does not establish the specific role of mitochondria in astrocytes located in the SNpc. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Bantle, C. M., Hirst, W. D., Weihofen, A., & Shlevkov, E.
Affiliations
Biogen (United States) (US)
Corresponding author
Shlevkov, Evgeny
Venue
Frontiers in Cell and Developmental Biology
Published
2021-01-07
Volume
8
Pages
608026-608026
ISSN
2296-634X (ISSN-L)
OpenAlex
W3118276045
Cited by
95
References
22
Citations by year
2026: 17 · 2025: 18 · 2024: 20 · 2023: 16 · 2022: 13 · 2021: 10 · 2020: 1
FWCI
1.89
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondrial dysfunction, astrocytes, Parkinson's disease, glutamate metabolism, calcium signaling, fatty acid metabolism, antioxidant production, neuroinflammation, glial cells, treatment development

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