The Alzheimer's disease mitochondrial cascade hypothesis: an update
Open accessAbstract
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.
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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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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 [148]
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“membrane protein, may associate with AD (Gunther et al., 2004; Belin et al., 2007; Alvarez et al., 2008; Bekris et al., 2008).”
BackgroundWidespread γ-secretase activity in the cell, but do we need it at the mitochondria?
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Khan (2000) · doi:10.1002/1531-8249(200008)48:2
Flagged first, then by citations
Research works printed but not linked: 1
- Lovestone S Reynolds CH 1997 The phosphorylation of tau: a critical stage in neurodevelopment and neurodegenerative processes Neuroscience 78 309 324 9145789
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Mitochondria and Mitochondrial Cascades in Alzheimer’s disease
Swerdlow, R. H. (2018) · Journal of Alzheimer’s Disease · doi:10.3233/jad-170585 · Cited by 850 · see citing works
Self-citationThe Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives
Swerdlow, R. H., Burns, J. M., & Khan, S. M. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.09.010 · Cited by 786 · see citing works
“This review will discuss recent AD biomarker data, diagnostic criteria, and clinical trial results from the perspective of a different AD hypothesis, the “mitochondrial cascade hypothesis” [21-27].”
BackgroundSelf-citationMitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology
Moreira, P. I., Carvalho, C., Zhu, X., Smith, M. A., & Perry, G. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.10.006 · Cited by 734 · see citing works
The Alzheimer’s Disease Mitochondrial Cascade Hypothesis
Swerdlow, R. H., Burns, J. M., & Khan, S. M. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100339 · Cited by 562 · see citing works
“In developing our hypothesis, we have therefore considered aging theory and how it may relate to late-onset AD [15,16].”
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Perez Ortiz, J. M., & Swerdlow, R. H. (2019) · British Journal of Pharmacology · doi:10.1111/bph.14585 · Cited by 426 · see citing works
Self-citationBrain aging, Alzheimer's disease, and mitochondria
Swerdlow, R. H. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.08.012 · Cited by 306 · see citing works
“An alternative to the amyloid cascade hypothesis [141 – 143], the mitochondrial cascade hypothesis [123,146 – 148], sees brain aging and AD as part of a continuum.”
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Self-citationProgressive regional atrophy in normal adults with a maternal history of Alzheimer disease
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Self-citationMosconi, L., de Leon, M., Murray, J., E, L., Lu, J., Javier, E., McHugh, P., & Swerdlow, R. H. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-110866 · Cited by 97 · see citing works
Neuron Specific Toxicity of Oligomeric Amyloid-β: Role for JUN-Kinase and Oxidative Stress
Ebenezer, P. J., Weidner, A. M., LeVine, H., Markesbery, W. R., Murphy, M. P., Zhang, L., Dasuri, K., Fernandez-Kim, S. O., Bruce-Keller, A. J., Gavilán, E., et al. (2010) · Journal of Alzheimer's Disease · doi:10.3233/jad-2010-101161 · Cited by 58 · see citing works
Mitochondrial medicine and the neurodegenerative mitochondriopathies
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Polymorphic variation in cytochrome oxidase subunit genes
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Self-citationMitochondrial Function and Neurodegenerative Diseases
Wilkins, H. M., Weidling, I., Koppel, S., Wang, X., von Schulze, A., & Swerdlow, R. H. (2018) · The Molecular and Cellular Basis of Neurodegenerative Diseases · doi:10.1016/b978-0-12-811304-2.00013-4 · Cited by 2 · see citing works
Self-citation
- Authors
- Swerdlow, R. H., & Khan, S. M.
- Affiliations
- University of Kansas (US)
- Gencia (United States) (US)
- Corresponding author
- Swerdlow, Russell H.
- ORCID
- Swerdlow, Russell H.
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 218
- Issue
- 2
- Pages
- 308-315
- ISSN
- 0014-4886 (ISSN-L)
- PMC
- PMC2710413
- OpenAlex
- W2023154785
- Cited by
- 206
- References
- 141
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 9 · 2023: 9 · 2022: 8 · 2021: 4 · 2020: 17 · 2019: 10 · 2018: 8 · 2017: 9 · 2016: 9 · 2015: 9 · 2014: 5 · 2013: 12 · 2012: 27
- FWCI
- 3.11
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG022407)
- 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
- Alzheimer's disease, sporadic Alzheimer's disease, autosomal dominant Alzheimer's disease, mitochondrial function, aging, heredity (biology), histopathology, disease threshold
- MeSH terms
- Aging, Alzheimer Disease, Amyloidosis, Animals, Brain, Cell Cycle, Humans, Mitochondria, Risk Factors, tau Proteins
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