ArticleNeurobiology of disease2022
SOD1 mediates lysosome-to-mitochondria communication and its dysregulation by amyloid-β oligomers.
Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 22 citations in OpenAlex.
- SOD1 co-pathologies in the brain: insights from neuropathological evidence and implications.Acta neuropathologica · 2026Review
- Retinal proteomics in neurodegeneration: Insights into ocular and brain disorders.Neural regeneration research · 2026Article
- Disease-specific tau polymorphs are associated with unique protein networks across proteinopathies.The EMBO journal · 2026Article
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- Mitochondrial NADK2-dependent NADPH controls tau oligomer uptake in human neurons.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Mitochondrial dysfunction and programmed cell death in Alzheimer's disease: A retrospective bioinformatics study.Medicine · 2026Article
- Beyond Antioxidants: How Redox Pathways Shape Cellular Signaling and Disease Outcomes.Antioxidants (Basel, Switzerland) · 2025Review
- Therapeutic Applications and Mechanisms of Superoxide Dismutase (SOD) in Different Pathogenesis.Biomolecules · 2025Review
- Triphenylphosphine-Based Mitochondrial Targeting Nanocarriers: Advancing Cancer Therapy.Clinical pharmacology : advances and applications · 2025Review
- Microglia degrade Alzheimer's amyloid-beta deposits extracellularly via digestive exophagy.Cell reports · 2024Article
- Unveiling biomarker detection in Alzheimer's disease: a computational approach to microarray analysis.3 Biotech · 2024Article
- Different amyloid β42 preparations induce different cell death pathways in the model of SH-SY5Y neuroblastoma cells.Cellular & molecular biology letters · 2024Article
- Disrupted mitochondrial response to nutrients is a presymptomatic event in the cortex of the APPAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Superoxide dismutase 1 mediates adaptation to the tumor microenvironment of glioma cells via mammalian target of rapamycin complex 1.Cell death discovery · 2024Article
- The role of TSC1 and TSC2 proteins in neuronal axons.Molecular psychiatry · 2024Review
- Mitochondrial metabolism in neural stem cells and implications for neurodevelopmental and neurodegenerative diseases.Journal of translational medicine · 2024Review
- Advancements in mitochondrial-targeted nanotherapeutics: overcoming biological obstacles and optimizing drug delivery.Frontiers in immunology · 2024Review
- Dysregulation of mTOR by tau in Alzheimer's disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- PNPLA3-I148M Variant Promotes the Progression of Liver Fibrosis by Inducing Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
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13 authors at 2 institutions in 1 country.
Funding
Abstract
Altered mitochondrial DNA (mtDNA) occurs in neurodegenerative disorders like Alzheimer's disease (AD); how mtDNA synthesis is linked to neurodegeneration is poorly understood. We previously discovered Nutrient-induced Mitochondrial Activity (NiMA), an inter-organelle signaling pathway where nutrient-stimulated lysosomal mTORC1 activity regulates mtDNA replication in neurons by a mechanism sensitive to amyloid-β oligomers (AβOs), a primary factor in AD pathogenesis (Norambuena et al., 2018). Using 5-ethynyl-2'-deoxyuridine (EdU) incorporation into mtDNA of cultured neurons, along with photoacoustic and mitochondrial metabolic imaging of cultured neurons and mouse brains, we show these effects being mediated by mTORC1-catalyzed T40 phosphorylation of superoxide dismutase 1 (SOD1). Mechanistically, tau, another key factor in AD pathogenesis and other tauopathies, reduced the lysosomal content of the tuberous sclerosis complex (TSC), thereby increasing NiMA and suppressing SOD1 activity and mtDNA synthesis. AβOs inhibited these actions. Dysregulation of mtDNA synthesis was observed in fibroblasts derived from tuberous sclerosis (TS) patients, who lack functional TSC and elevated SOD1 activity was also observed in human AD brain. Together, these findings imply that tau and SOD1 couple nutrient availability to mtDNA replication, linking mitochondrial dysfunction to AD.
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