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PreprintCC BY-NCbioRxiv

Cellular and mitochondrial correlates of regional glucose metabolism in the human cortex

  • M. Murgas
  • S. Habernig
  • C. Milz
  • S. Graf
  • M. B. Reed
  • B. Eggerstorfer
  • P. Falb
  • C. Schmidt
  • E. Briem
  • G. Schlosser
  • A. Mayerweg
  • K. Al Barede
7 more authors
  • I. Pörnbacher
  • L. Nics
  • S. Rasul
  • M. Hacker
  • D. Rujescu
  • A. Hahn
  • R. Lanzenberger1
  1. 1Department of Psychiatry and Psychotherapy, Clinical Division of General Psychiatry, Medical University of Vienna, Austria; Comprehensive Center for Clinical Ne
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Abstract

Regional differences in human brain glucose metabolism reflect local energy demands, but their cellular and mitochondrial determinants remain unclear. We combined [18F]FDG positron emission tomography in healthy human participants with estimates of cellular composition and mitochondrial density to unravel (sub)cellular correlates of heterogeneity in brain glucose metabolism. By correcting for RNA content and differential gene expression due to postmortem sampling, we addressed methodological shortcomings in multimodal neuroimaging integration. We introduce transcriptionally derived cytoarchitectonic maps of the human cortex that are consistent with histological findings, providing a biologically grounded framework for relating in vivo neuroimaging signals. Accordingly, mitochondrial distribution showed strong association with the intrinsic energy requirements at resting state. In contrast, relations between metabolism and neuronal composition were driven by sensory input and mitochondria-sparse thin-axon neurons, suggesting that stimulation-induced energy demand is met rather by neuronal processes that are independent of mitochondrial abundance to maintain efficient information processing.

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Cite

BibTeXRIS
BibTeX
@misc{murgas2026cellular,
  title = {{Cellular and mitochondrial correlates of regional glucose metabolism in the human cortex}},
  author = {M. Murgas and S. Habernig and C. Milz and S. Graf and M. B. Reed and B. Eggerstorfer and P. Falb and C. Schmidt and E. Briem and G. Schlosser and A. Mayerweg and K. Al Barede and I. Pörnbacher and L. Nics and S. Rasul and M. Hacker and D. Rujescu and A. Hahn and R. Lanzenberger},
  howpublished = {bioRxiv},
  year = {2026},
  month = oct,
  doi = {10.64898/2026.10.22.760701},
  url = {https://www.biorxiv.org/content/10.64898/2026.10.22.760701v1},
  note = {CC BY-NC},
}
RIS
TY  - UNPB
TI  - Cellular and mitochondrial correlates of regional glucose metabolism in the human cortex
AU  - M. Murgas
AU  - S. Habernig
AU  - C. Milz
AU  - S. Graf
AU  - M. B. Reed
AU  - B. Eggerstorfer
AU  - P. Falb
AU  - C. Schmidt
AU  - E. Briem
AU  - G. Schlosser
AU  - A. Mayerweg
AU  - K. Al Barede
AU  - I. Pörnbacher
AU  - L. Nics
AU  - S. Rasul
AU  - M. Hacker
AU  - D. Rujescu
AU  - A. Hahn
AU  - R. Lanzenberger
PY  - 2026
DA  - 2026/10/22
PB  - bioRxiv
DO  - 10.64898/2026.10.22.760701
UR  - https://www.biorxiv.org/content/10.64898/2026.10.22.760701v1
AB  - Regional differences in human brain glucose metabolism reflect local energy demands, but their cellular and mitochondrial determinants remain unclear. We combined [18F]FDG positron emission tomography in healthy human participants with estimates of cellular composition and mitochondrial density to unravel (sub)cellular correlates of heterogeneity in brain glucose metabolism. By correcting for RNA content and differential gene expression due to postmortem sampling, we addressed methodological shortcomings in multimodal neuroimaging integration. We introduce transcriptionally derived cytoarchitectonic maps of the human cortex that are consistent with histological findings, providing a biologically grounded framework for relating in vivo neuroimaging signals. Accordingly, mitochondrial distribution showed strong association with the intrinsic energy requirements at resting state. In contrast, relations between metabolism and neuronal composition were driven by sensory input and mitochondria-sparse thin-axon neurons, suggesting that stimulation-induced energy demand is met rather by neuronal processes that are independent of mitochondrial abundance to maintain efficient information processing.
ER  -