ReviewBiochimica et biophysica acta2012
A mitochondrial etiology of Alzheimer and Parkinson disease.
Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
166 citing papers in PubMed, 2 syntheses or guidelines pooled it, 303 citations in OpenAlex.
- Does protracted radon exposure play a role in the development of dementia?Environmental research · 2022Pooled it
- Multivariate meta-analyses of mitochondrial complex I and IV in major depressive disorder, bipolar disorder, schizophrenia, Alzheimer disease, and Parkinson disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Pooled it
- Trial
- Distinct age-related pattern of mitochondrial somatic mutations across multiple sclerosis phenotypes.Journal of neurology · 2026Article
- Potassium ion homeostasis modulates mitochondrial function.The Journal of cell biology · 2026Article
- Mass spectrometry analysis of young and aged mice and human Alzheimer's disease with Lewy body pathology using on-slide tissue digestion.Analytical and bioanalytical chemistry · 2026Article
- Adaptation of mtDNA content to endurance training, a cross-sectional study and an endurance training intervention.European journal of applied physiology · 2026Article
- Radiation-Induced Neurodegeneration.Biomedicines · 2026Review
- Toward common treatment strategies: convergent proteinopathies and mitochondrial dysfunction in Alzheimer's and Parkinson's diseases.Frontiers in neuroscience · 2026Review
- Comprehensive and In-Depth Molecular and Pathway Studies of the Hippocampus in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Article
- Transcriptome and DNA methylation analysis of the goat pineal gland during puberty.Scientific reports · 2025Article
- Human SIRT5 variants with reduced stability and activity do not cause neuropathology in mice.iScience · 2024Article
- A bibliometric and visual analysis of epigenetic research publications for Alzheimer's disease (2013-2023).Frontiers in aging neuroscience · 2024Review
- C17orf80 binds the mitochondrial genome to promote its replication.The Journal of cell biology · 2023Article
- Cerebral oxygen metabolism from MRI susceptibility.NeuroImage · 2023Review
- Review
- A Review of the Recent Advances in Alzheimer's Disease Research and the Utilization of Network Biology Approaches for Prioritizing Diagnostics and Therapeutics.Diagnostics (Basel, Switzerland) · 2022Review
- Impact of Micro- and Nanoplastics on Mitochondria.Metabolites · 2022Review
- Article
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
106 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
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe genetics and pathophysiology of Alzheimer Disease (AD) and Parkinson Disease (PD) appears complex. However, mitochondrial dysfunction is a common observation in these and other neurodegenerative diseases. SCOPE OF REVIEW: We argue that the available data on AD and PD can be incorporated into a single integrated paradigm based on mitochondrial genetics and pathophysiology. MAJOR
conclusionsRare chromosomal cases of AD and PD can be interpreted as affecting mitochondrial function, quality control, and mitochondrial DNA (mtDNA) integrity. mtDNA lineages, haplogroups, such haplogroup H5a which harbors the mtDNA tRNA(Gln) A8336G variant, are important risk factors for AD and PD. Somatic mtDNA mutations are elevated in AD, PD, and Down Syndrome and Dementia (DSAD) both in brains and also systemically. AD, DS, and DSAD brains also have reduced mtDNA ND6 mRNA levels, altered mtDNA copy number, and perturbed Aβ metabolism. Classical AD genetic changes incorporated into the 3XTg-AD (APP, Tau, PS1) mouse result in reduced forebrain size, life-long reduced mitochondrial respiration in 3XTg-AD males, and initially elevated respiration and complex I and IV activities in 3XTg-AD females which markedly declines with age. GENERAL SIGNIFICANCE: Therefore, mitochondrial dysfunction provides a unifying genetic and pathophysiology explanation for AD, PD, and other neurodegenerative diseases. This article is part of a Special Issue entitled Biochemistry of Mitochondria.
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.