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Mitochondria importance articles
Abstract-level scientific briefs on mitochondria preprints—structured for researchers and agents. Free in the browser. Machine JSON remains available via x402 for bots.
13 of 77 articles · updated 2026-08-08T16:01Z
- biorxiv2026-07-29score 95OXPHOSneurobiologytherapeutics
Why this mitochondrial dysfunction preprint matters: Ringer Loss in Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson′s Disease
This biorxiv preprint matters for mitochondria agents because it engages OXPHOS, neurobiology, therapeutics. Dysfunction-adjacent signals: dysfunction, ROS / oxidative stress, OXPHOS / ETC, disease context, neurodegeneration.
Source preprint: Ringer Loss in Drosophila Uncovers Mitochondrial Complex I Deficits Characteristic of Human Parkinson’s Disease
- biorxiv2026-07-28score 95neurobiologyredox biology
Why this mitochondrial dysfunction preprint matters: Corilagin attenuates high glucose-induced neurotoxicity and mitochondrial dysfunction through restoration of the AMPK-SI
This biorxiv preprint matters for mitochondria agents because it engages neurobiology, redox biology. Dysfunction-adjacent signals: dysfunction, ROS / oxidative stress, neurodegeneration.
Source preprint: Corilagin attenuates high glucose-induced neurotoxicity and mitochondrial dysfunction through restoration of the AMPK-SIRT1-PGC1α-TFAM signalling axis
- biorxiv2026-08-04score 93OXPHOSredox biologyneurobiology
Elevated cholesterol in APOE4 astrocytes drives mitochondrial cristae collapse and ATP synthase dysfunction
Scientific focus: OXPHOS, redox biology, neurobiology, structural biology. Core claim (from abstract): Here we show that elevated intracellular cholesterol in murine astrocytes expressing the Alzheimer’s disease risk variant APOE4 disrupts the inner mitochondrial membrane, manifesting as sparse, truncated cristae alongside an excess of cristae junction complexes. Dysfunction linkage: mitochondrial dysfunction; cell death; OXPHOS / ETC; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Elevated cholesterol in APOE4 astrocytes drives mitochondrial cristae collapse and ATP synthase dysfunction
- biorxiv2026-07-25score 83neurobiologytherapeutics
Why this mitochondrial dysfunction preprint matters: Elunetirom, a brain-targeted TRβ prodrug, promotes neuronal plasticity and mitochondrial biogenesis-related signaling in
This biorxiv preprint matters for mitochondria agents because it engages neurobiology, therapeutics. Dysfunction-adjacent signals: dysfunction, disease context.
Source preprint: Elunetirom, a brain-targeted TRβ prodrug, promotes neuronal plasticity and mitochondrial biogenesis-related signaling in primary neuronal cultures
- biorxiv2026-08-07score 78redox biologyneurobiologyimmunology
Age-dependent brain pigmentation drives early neuroinflammatory molecular signatures linked to neurodegeneration
Scientific focus: redox biology, neurobiology, immunology, aging. Core claim (from abstract): Elevated intracellular NM levels have been linked to neurodegeneration and PD-like phenotypes in experimental models. Dysfunction linkage: mitochondrial dysfunction; disease context; aging; neurodegeneration. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Age-dependent brain pigmentation drives early neuroinflammatory molecular signatures linked to neurodegeneration
- medrxiv2026-07-29score 77neurobiologyredox biology
Why this mitochondrial dysfunction preprint matters: Assessment of Glucose Metabolism In Vivo in the Human Frontal Lobe Using Interleaved 1 H and 13 C MRS at 7T: Toward Clin
This medrxiv preprint matters for mitochondria agents because it engages neurobiology, redox biology. Dysfunction-adjacent signals: dysfunction, disease context, neurodegeneration.
Source preprint: Assessment of Glucose Metabolism In Vivo in the Human Frontal Lobe Using Interleaved 1 H and 13 C MRS at 7T: Toward Clinical Translation
- biorxiv2026-08-04score 76metabolismneurobiology
A guanosine metabolism-bioenergetics intersection drives Parkinson’s disease
Scientific focus: metabolism, neurobiology. Core claim (from abstract): We show here that the reliance on these two purine-based metabolites intersect at another PD susceptibility gene that encodes nucleoside diphosphate kinase (NDK) which converts ATP into GTP. Dysfunction linkage: mitochondrial dysfunction; functional impairment; bioenergetics; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: A guanosine metabolism-bioenergetics intersection drives Parkinson’s disease
- biorxiv2026-07-31score 76OXPHOSredox biologymetabolism
Loss of neurofibromin alters adult metabolism via effects during a developmental critical period
Scientific focus: OXPHOS, redox biology, metabolism, neurobiology. Core claim (from abstract): Neurofibromatosis type 1 (OMIM 162200) is a genetic disorder that results from mutations in the NF1 gene and its encoded neurofibromin protein (Nf1). Dysfunction linkage: OXPHOS / ETC; disease context; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Loss of neurofibromin alters adult metabolism via effects during a developmental critical period
- biorxiv2026-07-31score 73redox biologymetabolismneurobiology
A Grape Seed Oligomeric Procyanidin Extract Reverses Diet-Induced Obesity Through Gut Microbiota Remodeling and Restoration of GLP-1, Gut…
Scientific focus: redox biology, metabolism, neurobiology, immunology. Core claim (from abstract): Background Obesity is a complex multifactorial disease associated with chronic low grade inflammation, gut microbiota dysbiosis, and impaired gut-brain communication. Dysfunction linkage: functional impairment; disease context; inflammation; systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: A Grape Seed Oligomeric Procyanidin Extract Reverses Diet-Induced Obesity Through Gut Microbiota Remodeling and Restoration of GLP-1, Gut-Brain, and Gut-Liver Signaling
- biorxiv2026-08-01score 64redox biologymetabolismneurobiology
Cross-species neural co-culture uncovers metabolic signatures of cellular crosstalk
Scientific focus: redox biology, metabolism, neurobiology, immunology. Core claim (from abstract): This increase in brain size evolved alongside advanced cognitive abilities as well as an elevated energetic demand. Dysfunction linkage: systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: Cross-species neural co-culture uncovers metabolic signatures of cellular crosstalk
- biorxiv2026-07-27score 53mtDNAneurobiologytherapeutics
Why this mitochondrial dysfunction preprint matters: Bioenergetic dysfunction and inflammation in hiPSC-derived astrocytes from m.14484T>C Leber’s Hereditary Optic Neuropath
This biorxiv preprint matters for mitochondria agents because it engages mtDNA, neurobiology, therapeutics. Dysfunction-adjacent signals: dysfunction, ROS / oxidative stress, mtDNA, disease context, neurodegeneration.
Source preprint: Bioenergetic dysfunction and inflammation in hiPSC-derived astrocytes from m.14484T>C Leber’s Hereditary Optic Neuropathy
- biorxiv2026-07-29score 39neurobiologyredox biology
Mitos importance brief: KIN-29 SIK regulates stress-induced sleep through mitochondrial redox signaling
This biorxiv preprint matters for mitochondria agents because it engages neurobiology, redox biology. Dysfunction-adjacent signals: ROS / oxidative stress.
Source preprint: KIN-29 SIK regulates stress-induced sleep through mitochondrial redox signaling
- biorxiv2026-07-29score 25neurobiology
Mitos importance brief: Transcriptional Profiling of Planarian Regeneration Habituating to Physiological Stressor Reveals Individual and Collective Dynamics
This biorxiv preprint matters for mitochondria agents because it engages neurobiology. Framing is largely mechanistic rather than explicit pathology.
Source preprint: Transcriptional Profiling of Planarian Regeneration Habituating to Physiological Stressor Reveals Individual and Collective Dynamics