A “mitochondrial cascade hypothesis” for sporadic Alzheimer’s disease

Swerdlow, Russell H; Khan, Shaharyar M

doi:10.1016/j.mehy.2003.12.045

Cited by 758Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

A “mitochondrial cascade hypothesis” for sporadic Alzheimer’s disease

Swerdlow, Russell H, Khan, Shaharyar M·2004·Medical Hypotheses

DOI 10.1016/j.mehy.2003.12.045

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Abstract

Alzheimer's disease (AD) includes etiologically heterogeneous disorders characterized by senile or presenile dementia, extracellular amyloid protein aggregations containing an insoluble amyloid precursor protein derivative, and intracytoplasmic tau protein aggregations. Recent studies also show excess neuronal aneuploidy, programmed cell death (PCD), and mitochondrial dysfunction. The leading AD molecular paradigm, the "amyloid cascade hypothesis", is based on studies of rare autosomal dominant variants and does not specify what initiates the common late-onset, sporadic form. We propose for late-onset, sporadic AD a "mitochondrial cascade hypothesis" that comprehensively reconciles seemingly disparate histopathologic and pathophysiologic features. In our model, the inherited, gene-determined make-up of an individual's electron transport chain sets basal rates of reactive oxygen species (ROS) production, which determines the pace at which acquired mitochondrial damage accumulates. Oxidative mitochondrial DNA, RNA, lipid, and protein damage amplifies ROS production and triggers three events: (1) a reset response in which cells respond to elevated ROS by generating the beta-sheet protein, beta amyloid, which further perturbs mitochondrial function, (2) a removal response in which compromised cells are purged via PCD mechanisms, and (3) a replace response in which neuronal progenitors unsuccessfully attempt to re-enter the cell cycle, with resultant aneuploidy, tau phosphorylation, and neurofibrillary tangle formation. In addition to defining a role for aging in AD pathogenesis, the mitochondrial cascade hypothesis also allows and accounts for histopathologic overlap between the sporadic, late-onset and autosomal dominant, early onset forms of the disease.

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Age-related mitochondrial decline initiates a downward spiral of energy failure, ROS accumulation, and altered APP metabolism.
“The mitochondrial cascade hypothesis, first proposed by Swerdlow and Khan [54], posits that age-related mitochondrial decline initiates a downward spiral of energy failure, reactive oxygen species (ROS) accumulation, and altered APP metabolism.”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [54]
According to the mitochondrial cascade hypothesis, Aβ is not an upstream biomarker of AD, but is instead a downstream marker of evolving mitochondrial dysfunction.
“According to the hypothesis Aβ is not an “upstream” biomarker of AD, but is instead a “downstream” marker of evolving mitochondrial dysfunction.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
Aβ deposition within an aging brain simply indicates critical age-related changes are occurring.
“Accordingly, Aβ deposition within an aging brain simply indicates critical age-related changes are occurring.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
According to the mitochondrial cascade hypothesis, mitochondrial function constitutes the crucial link between brain aging and AD.
“According to the mitochondrial cascade hypothesis, mitochondrial function constitutes the crucial link between brain aging and AD.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
The mitochondrial cascade hypothesis deviates from the amyloid cascade hypothesis by predicting age-related changes in mitochondrial function, rather than mutations or polymorphisms in APP or Aβ processing genes, primarily account for age-associated brain Aβ changes.
“It deviates from the amyloid cascade hypothesis by predicting age-related changes in mitochondrial function, rather than mutations or polymorphisms in APP or Aβ processing genes, primarily account for age-associated brain Aβ changes.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]

If the mitochondrial cascade hypothesis is correct, early-onset, autosomal dominant and late-onset, non-autosomal dominant AD cases do not share a common etiology.
“If correct, the mitochondrial cascade hypothesis has several inconvenient implications. The main implication is that early-onset, autosomal dominant and late-onset, non-autosomal dominant AD cases do not share a common etiology.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
Models based on early-onset, autosomal dominant AD may provide limited insight into late-onset, non-autosomal dominant AD.
“Models based on early-onset, autosomal dominant AD may therefore provide limited insight into late-onset, non-autosomal dominant AD.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
In the mitochondrial cascade hypothesis, toxic cascades in AD are not initiated by Aβ, but by mitochondria.
“In other words, toxic cascades in AD are not initiated by Aβ, but by mitochondria.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
Mitochondrial function declines with age.
“The mitochondrial cascade hypothesis proposes mitochondrial function declines with age, and this decline promotes some features of brain aging including Aβ accumulation.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
The mitochondrial cascade hypothesis views Aβ more as a downstream biomarker of brain aging than as the primary upstream Alzheimer's disease biomarker.
“In contrast to the amyloid cascade hypothesis, which views Aβ as the primary upstream AD biomarker, the mitochondrial cascade hypothesis in general sees Aβ more as a downstream biomarker of brain aging.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
When mitochondrial decline surpasses a threshold, compensatory mechanisms fail and late-onset Alzheimer's disease ensues.
“When mitochondrial decline surpasses a threshold compensatory mechanisms fail and late-onset AD ensues.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
The age-related decline in mitochondrial function promotes some features of brain aging, including Aβ accumulation.
“The mitochondrial cascade hypothesis proposes mitochondrial function declines with age, and this decline promotes some features of brain aging including Aβ accumulation.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [147]
Mitochondrial function declines with age and leads to increased production of reactive oxygen species.
“In this explanation, the mitochondrial function declines with age and leads to increased production of ROS [65,66].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [65]

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Untitled work
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Authors: Swerdlow, R. H., & Khan, S. M.
Affiliations: University of Virginia Health System (US)
Corresponding author: Swerdlow, Russell H
ORCID: Swerdlow, Russell H
Venue: Medical Hypotheses
Publisher: Elsevier BV
Published: 2004-01
Volume: 63
Issue: 1
Pages: 8-20
ISSN: 0306-9877 (ISSN-L)
DOI: 10.1016/j.mehy.2003.12.045
OpenAlex: W2141282621
Cited by: 758
References: 189
Citations by year: 2026: 45 · 2025: 44 · 2024: 51 · 2023: 50 · 2022: 52 · 2021: 57 · 2020: 63 · 2019: 56 · 2018: 37 · 2017: 31 · 2016: 37 · 2015: 31 · 2014: 33 · 2013: 28 · 2012: 21
FWCI: 9.07
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Medical Hypotheses (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: sporadic Alzheimer's disease, amyloid hypothesis, late-onset Alzheimer's disease, electron transport chain, reactive oxygen species, mitochondrial DNA damage, amyloid-beta, programmed cell death, tau phosphorylation, neurofibrillary tangles, aging, autosomal dominant Alzheimer's disease, mitochondrial dysfunction
MeSH terms: Aging, Alzheimer Disease, Brain, Humans, Mitochondria, Models, Biological, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, Reactive Oxygen Species, Mitochondrial Proteins, Mitochondrial Diseases

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A “mitochondrial cascade hypothesis” for sporadic Alzheimer’s disease

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