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The Alzheimer’s Disease Mitochondrial Cascade Hypothesis
Open accessAbstract
We first proposed the mitochondrial cascade hypothesis of sporadic Alzheimer's disease (AD) in 2004. Our core assumptions were a person's genes determine baseline mitochondrial function and durability, this durability determines how mitochondria change with advancing age, and critical changes in mitochondrial function initiate other pathologies characteristic of AD. Since then several lines of investigation report data consistent with or supportive of our hypothesis. In particular, AD endophenotype studies suggest a strong maternal genetic contribution, and links between mitochondrial function, tau phosphorylation, and amyloid-beta (Abeta) amyloidosis are increasingly recognized. As predicted, AD therapies designed to reduce Abeta thus far have had at best very limited clinical benefits; our hypothesis identifies alternative therapeutic targets. While placing mitochondria at the apex of an AD cascade certainly remains controversial, it is increasingly accepted by the AD research community that mitochondria play an important role in the late-onset forms of the disease. Even if the mitochondrial cascade hypothesis proves incorrect, considering its assumptions could potentially advance our understanding of sporadic, late-onset AD.
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In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [146]
In the citing paper
“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 [66]
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Citations
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Melatonin and Its Agonist Ramelteon in Alzheimer′s Disease: Possible Therapeutic Value
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CoQ10 and Mitochondrial Dysfunction in Alzheimer’s Disease
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“Such pathogenic signals would emerge from events such as an ageassociated accumulation of oxidative radicals, inherited mitochondrial DNA mutations, carriage of the APOE-e4 risk factor, among others [8, 27, 64].”
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“REVIEW ARTICLE oxidative stress, inflammation and altered mitochondrial function (Swerdlow et al., 2010).”
BackgroundTargeting Mitochondrial Bioenergetics for Alzheimers Prevention and Treatment
Yao, J., & Brinton, R. D. (2011) · Current Pharmaceutical Design · doi:10.2174/138161211798072517 · Cited by 50
Swerdlow, R. H. (2013) · British Journal of Pharmacology · doi:10.1111/bph.12394 · Cited by 51
“A ‘mitochondrial cascade hypothesis’ assumes this latter possibility (Swerdlow and Khan, 2004; Swerdlow and Khan, 2009; Swerdlow et al., 2010).”
BackgroundArrázola, M. S., Ramos‐Fernández, E., Cisternas, P., Ordenes, D., & Inestrosa, N. C. (2017) · PLoS ONE · doi:10.1371/journal.pone.0168840 · Cited by 49
Near infrared light decreases synaptic vulnerability to amyloid beta oligomers
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“A mitochondrial cascade hypothesis has been proposed and is increasingly invoked to understand the causes of sporadic AD; it is based on mitochondrial dysfunction due to oxidative stress and a correlation betweenadvancing age andAD risk (Swerdlow&Khan, 2004; Swerdlow et al, 2010).”
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“Until recently the role of mtDNA modifications in AD has been largely ignored, despite the 156 evidence that mitochondrial dysfunction is involved in AD [18] and that ncDNA methylation 157”
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“Mitochondrial Dysfunction and Oxidative Stress Mitochondrial dysfunction is an early event in AD pathogenesis (87).”
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“Impaired mitochondrial functions, oxidative stress and inflammatory processes have also been suggested to play a role in AD pathogenesis [76].”
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“Oxidative stress has been suggested to facilitate pathological aggregation of β-amyloid and tau, which are then believed to further damage mitochondria in a vicious cycle (Swerdlow et al., 2010; Leuner et al., 2012).”
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“Focusing on the mitochondria will identify alternative therapeutic targets that could lead to early therapeutic interventions [65].”
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“Deposition of Aβ plaques causes damage also to mitochondria with ROS production disrupting the electron transport chain (Swerdlow et al. 2010).”
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“A higher frequency of D310 heteroplasmy in the blood cells of LOAD patients compared to healthy controls was recently reported [6].”
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Impaired fasting glucose is associated with increased regional cerebral amyloid
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“This concept has been put forward in the “mitochondrial cascade hypothesis” first proposed more than 10 years ago by Swerdlow and coworkers [8, 38, 39].”
Mitoproteomics: Tackling Mitochondrial Dysfunction in Human Disease
Gómez‐Serrano, M., Camafeita, E., Loureiro, M., & Peral, B. (2018) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2018/1435934 · Cited by 38
“Causal links for mitochondrial abnormalities and oxidative damage in synaptic degeneration and amyloid-β deposition have been proposed [133, 134].”
BackgroundPeripheral and Central Glutamate Dyshomeostasis in Neurodegenerative Disorders
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“Currently the relationship of amyloid generation and toxicity to mitochondrial dysfunction in the brain is still unclear, with evidence for both a role of amyloid toxicity leading to mitochondrial abnormalities as well as a role for mitochondrial dysfunction exacerbating amyloid generation and toxicity [29].”
BackgroundTOMM40 and APOE Gene Expression and Cognitive Decline in Japanese Alzheimer’s Disease Subjects
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“When it comes to altered mitochondrial function in these conditions there are commonalities, such as the fact that changes are observed both within and beyond the nervous system and are therefore not simply a consequence of neurodegeneration [3, 4, 5].”
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“Series of experiments have suggested that activation of PPAR may act to improve mitochondrial functions, and this may be the basis of beneficial effects on memory and cognition (Mancuso et al. 2008; Swerdlow and Khan 2009; Swerdlow et al. 2010).”
BackgroundBioenergetics and metabolism: a bench to bedside perspective
Swerdlow, R. H. (2016) · Journal of Neurochemistry · doi:10.1111/jnc.13509 · Cited by 35
New Therapeutics to Modulate Mitochondrial Function in Neurodegenerative Disorders
Wilkins, H., & Morris, J. K. (2017) · Current Pharmaceutical Design · doi:10.2174/1381612822666161230144517 · Cited by 34
“mtDNA is almost entirely derived maternally, and those whose mother is afflicted with AD have a higher risk to develop AD [38, 39].”
BackgroundSwerdlow, R. H. (2011) · Antioxidants and Redox Signaling · doi:10.1089/ars.2011.3948 · Cited by 35
“While in some ways this will no doubt advance our knowledge of PD in general and especially our understanding of the Mendelian forms, overgeneralizations could prove dangerous and an over-reliance on Mendelian models could impede PD therapeutic development as it has in other fields (129, 132, 133).”
Asim, A., Jastrzębski, M. K., & Kaczor, A. A. (2025) · Molecules · doi:10.3390/molecules30142975 · Cited by 43
“The theory states that various mechanisms, including oxidative stress and proteasome dysfunction, facilitate mitochondrial dysfunction in neurodegenerative diseases such as AD [25].”
Protective effects of a small molecule inhibitor, DDQ against amyloid beta in Alzheimer’s disease
Vijayan, M., Bose, C., & Reddy, P. H. (2021) · Mitochondrion · doi:10.1016/j.mito.2021.04.005 · Cited by 34
Bell, S., Wareing, H. E., Capriglia, F., Hughes, R. M., Barnes, K., Hamshaw, A., Adair, L. D., Shaw, A. C., Olejnik, A., De, S., et al. (2024) · Molecular Psychiatry · doi:10.1038/s41380-024-02746-8 · Cited by 35
“This has led to the suggestion that metabolic failure, or reductions in metabolic ef fi ciency of brain cells may be a key step in the development of AD [11, 12].”
Differential transcriptome expression in human nucleus accumbens as a function of loneliness
Canli, T., Wen, R., Wang, X., Mikhailik, A., Yu, L., Fleischman, D. A., Wilson, R. S., & Bennett, D. A. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.186 · Cited by 33
“In this study cohort, a larger proportion of lonely than non-lonely individuals met pathologic criteria for AD at the time of death (our analyses controlled for AD status), and mitochondrial dysfunction may be the primary driver of AD pathology (57– 59).”
Ding, H., Reiss, A. B., Pinkhasov, A., & Kasselman, L. J. (2022) · Medicina · doi:10.3390/medicina58081025 · Cited by 32
“In addition to increased inflammation, which may be toxic long-term, AD has been associated with mitochondrial dysfunction, with changes in mitochondrial processing resulting in increased oxidative stress [19].”
BackgroundAtlante, A., & Valenti, D. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242115951 · Cited by 33
“Slowing of ETC leads to ROS formation at complex I [25,44,213], thus linking ETC inhibition and ROS accumulation in AD and suggesting that mitochondrial complex I dysfunction may contribute to the pathogenesis of sporadic AD.”
BackgroundSharma, Y., & Garabadu, D. (2020) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2020.08.020 · Cited by 31
Islam, M. S., Al‐Majid, A. M., Azam, M., Verma, V. P., Barakat, A., Haukka, M., Elgazar, A. A., Mira, A., & Badria, F. A.-E. (2021) · ACS Omega · doi:10.1021/acsomega.1c03978 · Cited by 32
Biomarkers associated with the pathogenesis of Alzheimer’s disease
Wang, H., Sun, M., Li, W., Liu, X., Zhu, M., & Qin, H. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1279046 · Cited by 35
“Early illness susceptibility is increased in individuals with low baseline mitochondrial function and a rapid reduction in function (Swerdlow and Khan, 2004; Swerdlow et al., 2010, 2018; Yang Y. et al., 2022; Swerdlow, 2023).”
BackgroundTOMM40 intron 6 poly‐T length, age at onset, and neuropathology of AD in individuals with APOE ɛ3/ɛ3
Li, G., Bekris, L. M., Leong, L., Steinbart, E. J., Shofer, J. B., Crane, P. K., Larson, E. B., Peskind, E. R., Bird, T. D., & Yu, C. (2012) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2012.06.009 · Cited by 30
The role of cell type-specific mitochondrial dysfunction in the pathogenesis of Alzheimer's disease
Kim, D., & Mook‐Jung, I. (2019) · BMB Reports · doi:10.5483/bmbrep.2019.52.12.282 · Cited by 31
“involved in the pathogenesis of AD (11, 12).”
BackgroundBroad activation of the Parkin pathway induces synaptic mitochondrial deficits in early tauopathy
Jeong, Y. Y., Han, S., Jia, N., Zhang, M., Sheshadri, P., Tammineni, P., Cheung, J., Nissenbaum, M., Baskar, S. S., Kwan, K. Y., et al. (2022) · UCL Discovery (University College London) · Cited by 32
Characterization of Mitochondrial DNA Methylation of Alzheimer’s Disease in Plasma Cell-Free DNA
Ding, B.-R., Zhang, X., Wan, Z.-Q., Tian, F., Ling, J., Tan, J.-Q., & Peng, X.-Q. (2023) · Diagnostics · doi:10.3390/diagnostics13142351 · Cited by 31
“The mitochondrial cascade hypothesis of AD [6] proposes that genetic changes in mitochondrial genes resulting in impaired mitochondrial function are considered a primary mechanism of AD pathogenesis.”
BackgroundAssociation between thyroid function and Alzheimer's disease: A systematic review
Figueroa, P. B. S., Ferreira, A. F. F., Britto, L. R., Doussoulin, A. P., & Torrão, A. D. S. (2021) · Metabolic Brain Disease · doi:10.1007/s11011-021-00760-1 · Cited by 28
Cuciniello, R., Luongo, D., Ferramosca, A., Lunetti, P., Aufiero, V. R., Crispi, S., Zara, V., Maurano, F., Filosa, S., & Bergamo, P. (2022) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2022.08.027 · Cited by 29
Novel CSF biomarkers to discriminate FTLD and its pathological subtypes
del Campo, M., Galimberti, D., Elias, N., Boonkamp, L., Pijnenburg, Y. A., van Swieten, J. C., Watts, K., Paciotti, S., Beccari, T., Hu, W., et al. (2018) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.629 · Cited by 30
Mitochondrial Haplotypes Associated with Biomarkers for Alzheimer’s Disease
Ridge, P. G., Koop, A., Maxwell, T. J., Bailey, M. H., Swerdlow, R. H., Kauwe, J. S. K., Honea, R. A., & Initiative, A. D. N. (2013) · PLoS ONE · doi:10.1371/journal.pone.0074158 · Cited by 30
“In this model, mitochondrial function declines with age, and at a certain level of cellular dysfunction, amyloid-b production and other histological changes typical of AD arise as a consequence of compensation, and failed compensation, leading to neurodegeneration [57–59].”
BackgroundAbtahi, S., Masoudi, R., & Haddadi, M. (2020) · Gene · doi:10.1016/j.gene.2020.144854 · Cited by 31
Nutraceutical based SIRT3 activators as therapeutic targets in Alzheimer's disease
Govindarajulu, M., Ramesh, S., Neel, L. T., Fabbrini, M., Buabeid, M. A., Fujihashi, A., Dwyer, D., Lynd, T. O., Shah, K., Mohanakumar, K. P., et al. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.104958 · Cited by 31
Coronas‐Samano, G., Baker, K. L., Tan, W. J. T., Ivanova, A. V., & Verhagen, J. V. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00268 · Cited by 29
“The result of these alterations may lead to Aβ accumulation, neuronal death, and dementia (Swerdlow et al., 2010).”
BackgroundChen, Z., Chen, L., Lyu, T., Weng, S., Xie, Y., Jin, Y., Wu, O., Jones, M., Kwan, K. Y.-H., Makvnadi, P., et al. (2024) · Acta Biomaterialia · doi:10.1016/j.actbio.2024.08.008 · Cited by 29
Hu, Y., Lai, J., Wan, B., Liu, X., Zhang, Y., Zhang, J., Sun, D., Ruan, G., Liu, E., Liu, G., et al. (2016) · NeuroToxicology · doi:10.1016/j.neuro.2016.02.012 · Cited by 28
“Apoptosis is known to be involved in AD neurodegeneration and progression (Swerdlow et al., 2010); therefore, we performed TUNEL staining to detect whether neuronal apoptosis was changed after ELF-MF treatment.”
MethodPetrov, D., Luque, M., Pedrós, I., Ettcheto, M., Abad, S., Pallàs, M., Verdaguer, E., Auladell, C., Folch, J., & Camins, A. (2015) · Molecular Neurobiology · doi:10.1007/s12035-015-9522-6 · Cited by 28
Zhang, F., Zhong, R., Qi, H., Li, S., Cheng, C., Liu, X., Liu, Y., & Le, W. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00314 · Cited by 29
“…changes are still unclear, Aβ and tau abnormality (Hardy and Selkoe, 2002; Iqbal et al., 2016), autophagy dysregulation (Li et al., 2010), mitochondrial dysfunction (Swerdlow et al., 2010) and neuroinflammation (Heppner et al., 2015) are believed to contribute to the pathogenesis of AD.”
BackgroundMitochondrial dysfunction and Alzheimer's disease: prospects for therapeutic intervention
Lim, J. W., Lee, J., & Pae, A. N. (2020) · BMB Reports · doi:10.5483/bmbrep.2020.53.1.279 · Cited by 28
Evaluation of respiratory chain activity in lymphocytes of patients with Alzheimer disease
Feldhaus, P., Fraga, D. B., Ghedim, F. V., De Luca, R. D., Bruna, T. D., Heluany, M., Matos, M. P., Ferreira, G. K., Jeremias, I. C., Heluany, C., et al. (2011) · Metabolic Brain Disease · doi:10.1007/s11011-011-9253-y · Cited by 27
δ-COP modulates Aβ peptide formation via retrograde trafficking of APP
Bettayeb, K., Chang, J. C., Luo, W., Aryal, S., Varotsis, D. F., Randolph, L. K., Netzer, W. J., Greengard, P., & Flajolet, M. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1604156113 · Cited by 26
Li, L., Li, Q., Lu, H.-L., Li, P., Song, Y., & Yang, R.-L. (2016) · Brain Research · doi:10.1016/j.brainres.2016.12.024 · Cited by 27
“Compelling evidence has indicated that mitochondrial dysfunction plays a critical role in AD pathophysiological progression (Swerdlow et al., 2010; Swerdlow, 2011).”
BackgroundWang, Y., Chio, C., Kuo, S., Yeh, C., Ma, J., Liu, W., Lin, M.-T., Lin, K., & Chang, C. (2022) · Molecular Neurobiology · doi:10.1007/s12035-022-02728-3 · Cited by 26
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“Mitochondria are organelles known to be affected in AD [99].”
BackgroundTorrão, A. D. S., Café-Mendes, C. C., Real, C. C., Hernandes, M. S., Ferreira, A. F. B., Santos, T. O., Chaves-Kirsten, G. P., Mazucanti, C. H., Ferro, E. S., Scavone, C., et al. (2012) · Brazilian Journal of Psychiatry · doi:10.1016/j.rbp.2012.08.004 · Cited by 27
Forlenza, O. V., Diniz, B. S., Teixeira, A. L., Stella, F., & Gattaz, W. F. (2013) · Brazilian Journal of Psychiatry · doi:10.1590/1516-4446-2012-3505 · Cited by 31
Mitochondria as a target for neuroprotection: implications for Alzheimer´s disease
Cardoso, S., Seiça, R. M. F., & Moreira, P. I. (2016) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2016.1205488 · Cited by 27
Gene Interactions in Human Disease Studies—Evidence Is Mounting
Singhal, P., Verma, S. S., & Ritchie, M. D. (2023) · Annual Review of Biomedical Data Science · doi:10.1146/annurev-biodatasci-102022-120818 · Cited by 26
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Effects of ketogenic diet on cognitive functions of mice fed high-fat-high-cholesterol diet
Lin, D.-T., Kao, N.-J., Cross, T.-W., Lee, W., & Lin, S. (2022) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2022.108974 · Cited by 29
Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders
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Sharma, P., & Singh, M. (2023) · Life Sciences · doi:10.1016/j.lfs.2023.121568 · Cited by 25
Preventing Alzheimer's disease by means of natural selection
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“This has led some to propose that bioenergetic failure in vulnerable neurons may be the primary driver of sporadic AD [44,45].”
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“A proteomic work on cerebral cortices of 6-month-old male 3 × Tg-AD (which harbor mutations in three human transgenes) analyzed before deposition of significant amyloid plaques and NFTs found derangement in protein expression in TCA enzymes and oxidative phosphorylation subunits, suggesting an early role of mitochondr…”
InfluentialGao, J., Qin, S., & Jiang, C. (2015) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmv044 · Cited by 24
“Abnormal mitochondrial function has been implicated in many neurodegenerative diseases, including Parkinson’s disease and Alzheimer’s disease [2,3].”
BackgroundJia, N., Ganesan, D., Guan, H., Jeong, Y. Y., Han, S., Rajapaksha, G., Nissenbaum, M., Kusnecov, A. W., & Cai, Q. (2024) · Autophagy · doi:10.1080/15548627.2024.2392408 · Cited by 27
Targeting Mitophagy in Alzheimer’s Disease
Jayatunga, D. P. W., Hone, E., Bharadwaj, P., Garg, M. L., Verdile, G., Guillemin, G. J., & Martins, R. N. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-191258 · Cited by 25
“According to the mitochondrial cascade hypothesis proposed by Swerdlow, Burns, and Khan [23, 170, 171], the bioenergetic deficit resulting from mitochondrial dysfunction is a primary event in the neurodegenerative process of AD.”
Metadata
- Authors
- Swerdlow, R. H., Burns, J. M., & Khan, S. M.
- Affiliations
- University of Kansas (US)
- Gencia (United States) (US)
- Corresponding author
- Swerdlow, Russell H.
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2010-06-03
- Volume
- 20
- Issue
- s2
- Pages
- S265-S279
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC2883665
- OpenAlex
- W1685999671
- Cited by
- 562
- References
- 145
- Citations by year
- 2026: 31 · 2025: 30 · 2024: 26 · 2023: 63 · 2022: 34 · 2021: 37 · 2020: 38 · 2019: 25 · 2018: 36 · 2017: 37 · 2016: 41 · 2015: 31 · 2014: 33 · 2013: 37 · 2012: 28
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Alzheimer s Disease (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG026374, R21AG029615, AG029615, AG022407, R01AG022407, R03AG026374)
- National Eye Institute (R21EY018474, EY018474)
- National Institute of Neurological Disorders and Stroke (K23NS058252)
- National Center for Research Resources (M01RR023940)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- MeSH terms
- Aging, Alzheimer Disease, Animals, Electron Transport Complex IV, DNA, Mitochondrial, Humans, Mitochondria, Models, Biological, Amyloid beta-Peptides
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