ReviewExperimental neurology2009
The Alzheimer's disease mitochondrial cascade hypothesis: an update.
Review in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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
112 citing papers in PubMed.
- Evaluating the causal effect of mitochondrial dysfunction on Alzheimer's disease and Parkinson's disease using polygenic risk scores and Mendelian randomization.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Region-specific ups and downs in mitochondrial numerical densities during Alzheimer's disease progression: A pilot study in human brains.Journal of Alzheimer's disease : JAD · 2026Article
- Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches.Journal of neuroscience research · 2025Review
- Efficacy of Transcranial Direct Current Stimulation and Photobiomodulation in Improving Cognitive Abilities for Alzheimer's Disease: A Systematic Review.Journal of clinical medicine · 2025Review
- Are current etiological theories of Alzheimer's disease falsifiable? An epistemological assessment.Frontiers in aging neuroscience · 2025Article
- Relationship between Alzheimer's Disease and Type 2 Diabetes: Critical Review On Cellular and Molecular Common Pathogenic Mechanisms.Current Alzheimer research · 2025Review
- MAMs and Mitochondrial Quality Control: Overview and Their Role in Alzheimer's Disease.Neurochemical research · 2024Review
- Biomaterials-based anti-inflammatory treatment strategies for Alzheimer's disease.Neural regeneration research · 2024Review
- A Scoping Review of Alzheimers Disease Hypotheses: An Array of Uni- and Multi-Factorial Theories.Journal of Alzheimer's disease : JAD · 2024Article
- Alzheimer's disease cortical morphological phenotypes are associated with TOMM40'523-APOE haplotypes.Neurobiology of aging · 2023Article
- The Effects of PP2A Disruption on ER-Mitochondria Contact and Mitochondrial Functions in Neuronal-like Cells.Biomedicines · 2023Article
- Article
- Article
- Diagnostic Accuracy of Blood-Based Biomarker Panels: A Systematic Review.Frontiers in aging neuroscience · 2022Article
- Mitochondrial Dysfunction in Alzheimer's Disease: Opportunities for Drug Development.Current neuropharmacology · 2022Article
- Brain simulation augments machine-learning-based classification of dementia.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- Mitochondria and Other Organelles in Neural Development and Their Potential as Therapeutic Targets in Neurodegenerative Diseases.Frontiers in neuroscience · 2022Review
- Amylin Pharmacology in Alzheimer's Disease Pathogenesis and Treatment.Current neuropharmacology · 2022Review
- TOMM40 and APOE variants synergistically increase the risk of Alzheimer's disease in a Chinese population.Aging clinical and experimental research · 2021Article
- Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.Cells · 2021Review
52 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
2 authors.
Funding
Abstract
In 2004 we proposed the mitochondrial cascade hypothesis of sporadic Alzheimer's disease (AD). Our hypothesis assumed sporadic and autosomal dominant AD are not etiologically homogeneous, considered evidence that AD pathology is not brain-limited, and incorporated aging theory. The mitochondrial cascade hypothesis asserted: (1) inheritance determines mitochondrial baseline function and durability; (2) mitochondrial durability influences how mitochondria change with age; and (3) when mitochondrial change reaches a threshold, AD histopathology and symptoms ensue. We now review the reasoning used to formulate the hypothesis, discuss pertinent interim data, and update its tenants. Readers are invited to consider the conceptual strengths and weaknesses of this hypothesis.
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.