ReviewAging and disease2016
Mitochondrial Dysfunction in Alzheimer's Disease and the Rationale for Bioenergetics Based Therapies.
Review in Aging and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07364162 (Exogenous Ketone Ester Supplementation in ICU Delirium), which is not on this map. Cited by 148 papers, 2 of them syntheses 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.
Exogenous Ketone Ester Supplementation in ICU Delirium (KETONES ICU)
Who cites it
148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 255 citations in OpenAlex.
- 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
- Protective Effects of Nicotinamide Adenine Dinucleotide and Related Precursors in Alzheimer's Disease: A Systematic Review of Preclinical Studies.Journal of molecular neuroscience : MN · 2021Pooled it
- Oxidative Stress and Dementia in Alzheimer's Patients: Effects of Synbiotic Supplementation.Oxidative medicine and cellular longevity · 2020Trial
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.Cells · 2026Review
- Targeting VDAC1 to protect against mitochondria-linked cell death pathways: apoptosis, pyroptosis, ferroptosis, and associated diseases.Apoptosis : an international journal on programmed cell death · 2026Article
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.Experimental neurology · 2026Article
- Early proteomic signatures of Alzheimer's disease in the retina and brain of 3xTg-AD mice.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanism of Alzheimer's disease using integrated multi-omics.Frontiers in aging neuroscience · 2026Review
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Early proteomic signatures of Alzheimer's disease in the retina and brain of 3xTg-AD mice.Frontiers in cell and developmental biology · 2026Article
- Redox Regulation of Complement Pathway Activation in Aging and Related Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- Potential therapeutic benefit of exogenous ketone ester administration in delirium: a narrative review.Critical care (London, England) · 2025Review
- Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- Integrated Multi-Omics Analysis and Cross-Model Validation Reveal Mitochondrial Signatures in Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- Review
- Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Mitochondrial dysfunction mediated by ER-calcium dysregulation in neurons derived from Alzheimer's disease patients.Acta neuropathologica communications · 2025Article
- Effect of neuroinflammation on the progression of Alzheimer's disease and its significant ramifications for novel anti-inflammatory treatments.IBRO neuroscience reports · 2025Review
88 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by the progressive loss of cholinergic neurons, leading to the onset of severe behavioral, motor and cognitive impairments. It is a pressing public health problem with no effective treatment. Existing therapies only provide symptomatic relief without being able to prevent, stop or reverse the pathologic process. While the molecular basis underlying this multifactorial neurodegenerative disorder remains a significant challenge, mitochondrial dysfunction appears to be a critical factor in the pathogenesis of this disease. It is therefore important to target mitochondrial dysfunction in the prodromal phase of AD to slow or prevent the neurodegenerative process and restore neuronal function. In this review, we discuss mechanisms of action and translational potential of current mitochondrial and bioenergetic therapeutics for AD including: mitochondrial enhancers to potentiate energy production; antioxidants to scavenge reactive oxygen species and reduce oxidative damage; glucose metabolism and substrate supply; and candidates that target apoptotic and mitophagy pathways to remove damaged mitochondria. While mitochondrial therapeutic strategies have shown promise at the preclinical stage, there has been little progress in clinical trials thus far.
Indexed as
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.