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Mitochondrial malfunction and atrophy of astrocytes in the aged human cerebral cortex

Author

Listed:
  • Alexander Popov

    (Jiaxing University
    Russian Academy of Sciences)

  • Nadezda Brazhe

    (Russian Academy of Sciences
    Moscow State University)

  • Kseniia Morozova

    (Moscow State University)

  • Konstantin Yashin

    (Privolzhskiy Research Medical University)

  • Maxim Bychkov

    (Russian Academy of Sciences)

  • Olga Nosova

    (Institute of Experimental Medicine)

  • Oksana Sutyagina

    (Russian Academy of Sciences)

  • Alexey Brazhe

    (Russian Academy of Sciences
    Moscow State University)

  • Evgenia Parshina

    (Moscow State University)

  • Li Li

    (Jiaxing University)

  • Igor Medyanik

    (Privolzhskiy Research Medical University)

  • Dmitry E. Korzhevskii

    (Institute of Experimental Medicine)

  • Zakhar Shenkarev

    (Russian Academy of Sciences)

  • Ekaterina Lyukmanova

    (Russian Academy of Sciences
    Moscow State University
    Shenzhen MSU-BIT University)

  • Alexei Verkhratsky

    (The University of Manchester
    IKERBASQUE, Basque Foundation for Science
    University of the Basque Country UPV/EHU and CIBERNED)

  • Alexey Semyanov

    (Jiaxing University
    Russian Academy of Sciences
    Moscow State University
    Sechenov First Moscow State Medical University)

Abstract

How aging affects cells of the human brain active milieu remains largely unknown. Here, we analyze astrocytes and neurons in the neocortical tissue of younger (22–50 years) and older (51–72 years) adults. Aging decreases the amount of reduced mitochondrial cytochromes in astrocytes but not neurons. The protein-to-lipid ratio decreases in astrocytes and increases in neurons. Aged astrocytes show morphological atrophy quantified by the decreased length of branches, decreased volume fraction of leaflets, and shrinkage of the anatomical domain. Atrophy correlates with the loss of gap junction coupling between astrocytes and increased input resistance. Aging is accompanied by the upregulation of glial fibrillary acidic protein (GFAP) and downregulation of membrane-cytoskeleton linker ezrin associated with leaflets. No significant changes in neuronal excitability or spontaneous inhibitory postsynaptic signaling is observed. Thus, brain aging is associated with the impaired morphological presence and mitochondrial malfunction of cortical astrocytes, but not neurons.

Suggested Citation

  • Alexander Popov & Nadezda Brazhe & Kseniia Morozova & Konstantin Yashin & Maxim Bychkov & Olga Nosova & Oksana Sutyagina & Alexey Brazhe & Evgenia Parshina & Li Li & Igor Medyanik & Dmitry E. Korzhevs, 2023. "Mitochondrial malfunction and atrophy of astrocytes in the aged human cerebral cortex," Nature Communications, Nature, vol. 14(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-44192-0
    DOI: 10.1038/s41467-023-44192-0
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    References listed on IDEAS

    as
    1. David Vilchez & Isabel Saez & Andrew Dillin, 2014. "The role of protein clearance mechanisms in organismal ageing and age-related diseases," Nature Communications, Nature, vol. 5(1), pages 1-13, December.
    2. Humsa S. Venkatesh & Wade Morishita & Anna C. Geraghty & Dana Silverbush & Shawn M. Gillespie & Marlene Arzt & Lydia T. Tam & Cedric Espenel & Anitha Ponnuswami & Lijun Ni & Pamelyn J. Woo & Kathryn R, 2019. "Electrical and synaptic integration of glioma into neural circuits," Nature, Nature, vol. 573(7775), pages 539-545, September.
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