ReviewInternational review of neurobiology2020
The mitochondrial hypothesis: Dysfunction, bioenergetic defects, and the metabolic link to Alzheimer's disease.
Review in International review of neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.
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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
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Mitochondrial dysfunction, oxidative stress, neuroinflammation, and metabolic alterations in the progression of Alzheimer's disease: A meta-analysis of in vivo magnetic resonance spectroscopy studies.Ageing research reviews · 2021Pooled it
- Effects of the SGLT2 inhibitor dapagliflozin in early Alzheimer's disease: A randomized controlled trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- An Alternative Metabolic Pathway of Glucose Oxidation Induced by Mitochondrial Complex I Inhibition: Serinogenesis and Folate Cycling.International journal of molecular sciences · 2025Article
- The absence of Parkin in hTau mice leads to synaptic mitochondrial dysfunction, alterations to the synaptic proteome, and increased phosphorylated tau in the Hippocampus.Neurobiology of disease · 2025Article
- Bioenergetic failure and oxidative stress: mitochondrial contributions to Alzheimer's disease.Inflammopharmacology · 2025Review
- Reliable New Biomarkers of Mitochondrial Oxidative Stress and Neuroinflammation in Cerebrospinal Fluid and Plasma from Alzheimer's Disease Patients: A Pilot Study.International journal of molecular sciences · 2025Article
- Impact of O-GlcNAcylation Elevation on Mitophagy and Glia in the Dentate Gyrus.Journal of neurochemistry · 2025Article
- A Narrative Review Evaluating Diet and Exercise as Complementary Medicine for the Management of Alzheimer's Disease.Nutrients · 2025Review
- Mitochondrial dynamics and bioenergetics in Alzheimer's induced pluripotent stem cell-derived neurons.Brain : a journal of neurology · 2025Article
- Functional Analysis of Direct In Vitro Effect of Phosphorylated Tau on Mitochondrial Respiration and Hydrogen Peroxide Production.Biomolecules · 2025Article
- Targeting Various Pathogenic Pathways for the Development of Anti-alzheimer's Drugs: An Update.Current topics in medicinal chemistry · 2025Review
- Rock inhibitors in Alzheimer's disease.Frontiers in aging · 2025Review
- Epigenetic regulation of the respiratory chain by a mitochondrial distress-related redox signal.Frontiers in cell and developmental biology · 2025Article
- Quantitative analysis of serum metabolites in a rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Epigenetic Threads of Neurodegeneration: TFAM's Intricate Role in Mitochondrial Transcription.CNS & neurological disorders drug targets · 2025Review
- Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Presenilin2 D439A Mutation Induces Dysfunction of Mitochondrial Fusion/Fission Dynamics and Abnormal Regulation of GTPase Activity.Molecular neurobiology · 2024Article
- ANU-ADRI scores, tau pathology, and cognition in non-demented adults: the CABLE study.Alzheimer's research & therapy · 2024Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) features mitochondrial dysfunction and altered metabolism. Other pathologies could drive these changes, or alternatively these changes could drive other pathologies. In considering this question, it is worth noting that perturbed AD patient mitochondrial and metabolism dysfunction extend beyond the brain and to some extent define a systemic phenotype. It is difficult to attribute this systemic phenotype to brain beta-amyloid or tau proteins. Conversely, mitochondria increasingly appear to play a critical role in cell proteostasis, which suggests that mitochondrial dysfunction may promote protein aggregation. Mitochondrial and metabolism-related characteristics also define AD endophenotypes in cognitively normal middle-aged individuals, which suggests that mitochondrial and metabolism-related AD characteristics precede clinical decline. Genetic analyses increasingly implicate mitochondria and metabolism-relevant genes in AD risk. Collectively these factors suggest that mitochondria are more relevant to the causes of AD than its consequences, and support the view that a mitochondrial cascade features prominently in AD. This chapter reviews the case for mitochondrial and metabolism dysfunction in AD and the challenges of proving that a primary mitochondrial cascade is pertinent to the disease.
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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.