ArticlebioRxiv : the preprint server for biology2025
Mitochondrial Energy Transformation Capacity Influences Brain Activation During Sensory, Affective, and Cognitive Tasks.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Plasma and cerebrospinal fluid proteomics reveal distinct patterns of senescence and neuropathology in aging rhesus macaques.GeroScience · 2026Article
- Chronic stress and the mitochondria-telomere axis: human evidence for a bioenergetic-debt model of early aging.Biogerontology · 2026Review
- Aging as the wound that fails to heal: a bioenergetic continuum of resolution failure.Biogerontology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Brain function relies on energy supplied by mitochondrial energy transformation, but how cellular energetics constrains neurological function and cognition remains poorly understood. Genetic defects in mitochondrial DNA cause rare mitochondrial diseases (MitoD) that offer a unique window to examine how mitochondria affects the brain and cognition, and the possibility to identify neural processes that are most energetically constrained. In this study, we assessed functional magnetic resonance imaging (fMRI) on 29 participants with MitoD and 62 matched controls during resting state and tasks probing cognitive (N-back task), affective (cold pain), and sensory (multisensory visual and auditory perception) functions. MitoD individuals exhibited significant cognitive deficits across a range of functions, including executive function and working memory, mental and physical fatigability, low exercise tolerance, and low mood. As expected, these deficits were accompanied by markedly elevated blood levels of metabolic stress markers, including GDF15 and FGF21. Surprisingly, overall BOLD fMRI activity and connectivity were largely intact across all tasks in MitoD individuals. However, those with more severe cognitive impairment and higher GDF15 levels showed reduced working memory-related BOLD activity, which in turn mediated poorer task performance. Conversely, individuals with relatively preserved cognitive function exhibited hyperactivation in working memory regions and working memory performance compared to controls, suggesting compensatory engagement of cortical systems in high-functioning MitoD individuals. These effects were weaker in the sensory domain and absent during affective (cold pain) processing. These data suggest that when mitochondrial energy transformation is limited, the brain operates an energy hierarchy that prioritizes essential functions such as affective responses while downregulating more energy-demanding, complex cognitive processes.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.