ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2014
Mitochondrial DNA deletions in Alzheimer's brains: a review.
Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- Article
- Therapeutic potential of melatonin-induced mitophagy in the pathogenesis of Alzheimer's disease.Inflammopharmacology · 2025Review
- Common mitochondrial deletions in RNA-Seq: evaluation of bulk, single-cell, and spatial transcriptomic datasets.Communications biology · 2024Article
- Probing the diagnostic values of plasma cf-nDNA and cf-mtDNA for Parkinson's disease and multiple system atrophy.Frontiers in neuroscience · 2024Article
- Review
- The Role of Bioenergetics in Neurodegeneration.International journal of molecular sciences · 2022Review
- Implication of Adult Hippocampal Neurogenesis in Alzheimer's Disease and Potential Therapeutic Approaches.Cells · 2022Review
- Hypermethylation of Mitochondrial Cytochrome b and Cytochrome c Oxidase II Genes with Decreased Mitochondrial DNA Copy Numbers in the APP/PS1 Transgenic Mouse Model of Alzheimer's Disease.Neurochemical research · 2021Article
- Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis.International journal of molecular sciences · 2021Review
- The Links between Cardiovascular Diseases and Alzheimer's Disease.Current neuropharmacology · 2021Review
- Novel Insights and Current Evidence for Mechanisms of Atherosclerosis: Mitochondrial Dynamics as a Potential Therapeutic Target.Frontiers in cell and developmental biology · 2021Review
- Insight into the genetic etiology of Alzheimer's disease: A comprehensive review of the role of rare variants.Alzheimer's & dementia (Amsterdam, Netherlands) · 2021Review
- The Dawn of Mitophagy: What Do We Know by Now?Current neuropharmacology · 2021Review
- Mitochondria dysfunction in the pathogenesis of Alzheimer's disease: recent advances.Molecular neurodegeneration · 2020Review
- Comparative functional genomic analysis of Alzheimer's affected and naturally aging brains.PeerJ · 2020Article
- Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas.The Journal of clinical investigation · 2019Review
- Mitochondrial Movement and Number Deficits in Embryonic Cortical Neurons from 3xTg-AD Mice.Journal of Alzheimer's disease : JAD · 2019Article
- Mitochondrial Targeting in Neurodegeneration: A Heme Perspective.Pharmaceuticals (Basel, Switzerland) · 2018Review
- The mitochondrial transcription factor TFAM in neurodegeneration: emerging evidence and mechanisms.FEBS letters · 2018Review
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 3 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction and increased oxidative stress have been associated with normal aging and are possibly implicated in the etiology of late-onset Alzheimer's disease (AD). DNA deletions, as well as other alterations, can result from oxidative damage to nucleic acids. Many studies during the past two decades have investigated the incidence of mitochondrial DNA deletions in postmortem brain tissues of late-onset AD patients compared with age-matched normal control subjects. Published studies are not entirely concordant, but their differences might shed light on the heterogeneity of AD itself. Our understanding of the role that mitochondrial DNA deletions play in disease progression may provide valuable information that could someday lead to a treatment.
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.