ReviewBiomedicines2021
Mitochondrial Dysfunction in Alzheimer's Disease: A Biomarker of the Future?
Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Quantitative assessment of efficacy and evaluation of feasibility of exercise training protocols in adult and pediatric primary mitochondrial disease.BMC medicine · 2026Pooled it
- An Integrated Analysis of Manganese Metabolism-Related Genes and Their Association With Biomarkers, Immune Infiltration, and Clinical Subtypes in Alzheimer's Disease.Genes, brain, and behavior · 2026Article
- Review
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Functional Implications of Marine Biosurfactants and Their Therapeutic Potential Against Alzheimer's Disease.Food science & nutrition · 2026Review
- Plasma Proteomic Networks Reveal Shared Biology with Brain Linked to Alzheimer's Disease Pathology.medRxiv : the preprint server for health sciences · 2026Article
- Peripheral Mitochondrial Energetics are Associated with Cortical Neurophysiological Alterations in Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2026Article
- Immunohistochemical Markers of Mitochondrial Electron Transport Chain Instability in Human Brain Regions: A Study of Aging and Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Simufilam in Alzheimer's Disease: Assessment of Efficacy of a Controversial Drug in Human Neuronal Cell Culture.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Sim-to-Real Domain Adaptation for Early Alzheimer's Detection from Handwriting Kinematics Using Hybrid Deep Learning.Sensors (Basel, Switzerland) · 2026Article
- Unraveling changes in mitochondrial processes influenced by ancestry inFrontiers in aging neuroscience · 2026Article
- Mitochondrial dysfunction in Alzheimer's disease: connecting pathophysiology with neuroimaging.Frontiers in aging neuroscience · 2026Review
- Article
- Molecular links between inflammatory bowel disease and Alzheimer's disease through immune signaling and inflammatory pathways.World journal of gastroenterology · 2025Review
- Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer's disease.Science advances · 2025Article
- Mitochondrial-Derived Peptides: Implication in the Therapy of Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Mapping key mitochondrial genes in Alzheimer's disease through human tissue and iPSC derived neurons.Scientific reports · 2025Article
- Orthobiologics and Peptide Therapy for Central Nervous System Repair in Neurodegenerative Conditions.Cells · 2025Review
- Age-Related Complement C3 Drives Memory Impairments and Associated Neuropathologies in a Mouse Model.Aging cell · 2025Article
- Potentiation of mitochondrial function by mitoDREADD-GNature neuroscience · 2025Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia worldwide and is characterised pathologically by the accumulation of amyloid beta and tau protein aggregates. Currently, there are no approved disease modifying therapies for clearance of either of these proteins from the brain of people with AD. As well as abnormalities in protein aggregation, other pathological changes are seen in this condition. The function of mitochondria in both the nervous system and rest of the body is altered early in this disease, and both amyloid and tau have detrimental effects on mitochondrial function. In this review article, we describe how the function and structure of mitochondria change in AD. This review summarises current imaging techniques that use surrogate markers of mitochondrial function in both research and clinical practice, but also how mitochondrial functions such as ATP production, calcium homeostasis, mitophagy and reactive oxygen species production are affected in AD mitochondria. The evidence reviewed suggests that the measurement of mitochondrial function may be developed into a future biomarker for early AD. Further work with larger cohorts of patients is needed before mitochondrial functional biomarkers are ready for clinical use.
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Identifiers
What OpenQuestion holds
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.