Mitochondrial alterations Alzheimer's disease
Open accessAbstract
Morphological alterations of mitochondria may be related to metabolic and energy deficiency in neurons in Alzheimer's disease (AD) and other neurodegenerative disorders. In previous studies on the morphological and morphometric estimation of mitochondria in AD, electron microscopy revealed substantial morphological and morphometric changes in the hippocampus, the acoustic cortex, the frontal cortex, and the cerebellum. This study extends this observation to subcortical centers, namely the thalamus, the globus pallidus, the red nucleus, and the locus caeruleus in 10 brains of patients who suffered from AD. The morphological alterations consisted of very obvious changes of the mitochondrial cristae, accumulation of osmiophilic material and decrease of their size, in comparison with the normal controls. Mitochondrial alterations were particularly prominent in neurons, which showed loss of dendritic spines and abbreviation of the dendritic arborization. The ultrastructural study of a large number of neurons in the thalamus and the red nucleus revealed that the mitochondrial alterations did not coexist with cytoskeletal pathology and accumulation of amyloid deposits. However, they were prominent in neurons, which demonstrated fragmentation of the cisternae of the Golgi apparatus. The morphological alterations of the mitochondria presumably suggest oxidative damage in neurons in AD brains.
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Dysregulated mitochondrial biogenesis, altered mitochondrial dynamics, and compromised genome integrity contribute to breakdown of mitochondrial health and function and are linked to Alzheimer's disease.
“Dysregulated mitochondrial biogenesis, alterations in mitochondrial dynamics (fusion and fission), and compromised genome integrity mechanisms collectively contribute to the breakdown of mitochondrial health and function. These factors are intricately linked to various disorders, notably AD (Baloyannis et al, 2004; Zhunina et al, 2020).”
From The mitochondrial long non-coding RNA lncMtloop regulates mitochondrial transcription and suppresses Alzheimer’s disease (2024) · cites this paper as Baloyannis et al, 2004
The Introduction links mitochondrial DNA defects and abnormal mitochondrial morphology to Alzheimer’s disease, and the Discussion links mitochondrial alterations to dysfunction. The paper does not establish dysregulated biogenesis or impaired fusion and fission as contributors to AD; fusion and fission appear only in a reference title. It discusses mtDNA defects, but not compromised genome-integrity mechanisms specifically. Page numbers were not available in our copy. (LLM, conf=0.88)
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“This is best illustrated by the myriad of mitochondrial-based diseases including Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis which are characterized by irregular mitochondrial structure and function ( Baloyannis et al. 2004; Dupuis et al. 2004; Stichel et al. 2007).”
BackgroundCell competition from development to neurodegeneration
RODRIGUES, M. C., Couceiro, J., & Moreno, E. (2021) · Disease Models & Mechanisms · doi:10.1242/dmm.048926 · Cited by 22 · see citing works
The role of GRASPs in morphological alterations of Golgi apparatus: mechanisms and effects
Ji, G., Ji, H., Mo, X.-Y., Li, T.-B., Yu, Y.-D., & Hu, Z.-P. (2013) · Reviews in the Neurosciences · doi:10.1515/revneuro-2013-0020 · Cited by 14
Youssef, Y. A., Tammam, S. N., El-Shenawy, B. M., Ilyas, S., Gad, A. A., Farag, K. S., Mathur, S., & Abdel-Kader, R. M. (2025) · European Journal of Pharmaceutics and Biopharmaceutics · doi:10.1016/j.ejpb.2025.114778 · Cited by 11 · see citing works
The role of mitochondrial remodeling in neurodegenerative diseases
Guan, D., Liang, C., Zheng, D., Liu, S., Luo, J., Cai, Z., Zhang, H., & Chen, J. (2025) · Neurochemistry International · doi:10.1016/j.neuint.2024.105927 · Cited by 11 · see citing works
MacDonald, J. A., Fowle, W., & Woods, D. (2017) · Micron · doi:10.1016/j.micron.2017.05.002 · Cited by 11 · see citing works
Targeting mitochondrial dysfunction in Alzheimer's disease: New findings and perspectives
Hroudová, J., & Fišar, Z. (2025) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2025.111491 · Cited by 9 · see citing works
Dentoni, G., Naia, L., Portal, B., Leal, N. S., Nilsson, P., Lindskog, M., & Ankarcrona, M. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220383 · Cited by 12 · see citing works
“Mitochondrial function is increased, and glycolytic reserve is decreased in App NL − F cultures A (cid:2) has been shown to mediate a variety of deleterious effects on mitochondria [38], and therefore we decided to characterize mitochondrial function in App NL − F cells.”
Tortuous Paths of Insulin Signaling and Mitochondria in Alzheimer’s Disease
Carvalho, C., Cardoso, S., Correia, S. C., & Moreira, P. I. (2019) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-3540-2_9 · Cited by 9 · see citing works
Wang, Y.-W., Huo, T., Tseng, Y.-J., Dang, L., Yu, Z.-L., Yu, W.-J., Foulks, Z., Murdaugh, R. L., Ludtke, S., Nakada, D., et al. (2022) · Communications Biology · doi:10.1038/s42003-022-03009-4 · Cited by 7 · see citing works
Mitochondria and Alzheimer’s Disease: An Electron Microscopy Study
Balogiannis, S. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.84881 · Cited by 8 · see citing works
“Among the many hypothesis, the most mattering are (a) the amyloid hypothesis [39, 40], (b) the metabolic and synaptic dysfunction hypothesis [41], (c) the hypothesis of translational neurodegeneration [42], (d) the tau hypothesis [43], (e) the hypothesis of neuroinflammation [44], (f) the cholinergic hypothesis [45],…”
BackgroundSelf-citationThe impact of exercise on brain mitochondrial health and its relevance to Alzheimer's disease
Csikós, V., Thyfault, J. P., & Wilkins, H. (2025) · Brain and Environment · doi:10.1016/j.braen.2025.100012 · Cited by 6 · see citing works
“Additionally, evidence suggests that mitochondrial dysfunction can occur before A β accumulation and cognitive decline, emphasizing its critical role in AD development (Baloyannis et al., 2004, Beal et al., 1993, Zhu et al., 2013, Yao et al., 2009).”
Lee, J., Park, H. J., Kang, S., Lee, S.-H., & Lee, C. K. (2024) · PLoS ONE · doi:10.1371/journal.pone.0306656 · Cited by 4
Targeting cellular batteries for the therapy of neurological diseases
Arora, A., Behl, T., Sehgal, A., Singh, S., Sharma, N., Mathew, B., & BUNGAU, S. G. (2021) · Environmental Science and Pollution Research · doi:10.1007/s11356-021-14665-0 · Cited by 5 · see citing works
What has Electron Microscopy Contributed to Alzheimer's Research?
Balogiannis, S. (2015) · Future Neurology · doi:10.2217/fnl.15.44 · Cited by 5 · see citing works
Self-citationCryo-ET distinguishes platelets during pre-acute myeloid leukemia from steady state hematopoiesisPreprint
Wang, Y.-W., Huo, T., Tseng, Y.-J., Dang, L. T. H., Yu, Z.-L., Yu, W.-Q., Foulks, Z., Ludtke, S., Nakada, D., & Wang, Z. (2021) · bioRxiv · doi:10.1101/2021.10.18.464863 · Cited by 2 · see citing works
An Individualized Approach to Treatment for Alzheimer’s Disease, Pick’s Disease, and Other Dementias
Lippa, C. F. (2006) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317506292372 · Cited by 2 · see citing works
“These signals are controlled by both genetic and environmental factors, and we are just beginning to understand the key interactions such as the relationship between Αβ or mitochondrial dysfunction and apoptotic cascades.(50,51) Studies of these cascades in large numbers of normal and degenerative disease subjects wou…”
BackgroundChakrabarti, S., & Sinha, M. S. (2012) · Springer eBooks · doi:10.1007/978-94-007-5237-5_4 · Cited by 1 · see citing works
Baloyannis, S. J. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.98436
Self-citationMitochondria as a Therapeutic Target for Alzheimer's Disease
Hung, C. H.-L., Cheng, S. S., Lee, S. M., & Chang, R. C. (2015) · Wiley eBooks · doi:10.1002/9781119017127.ch15
Peng, J., Zeng, F., He, Y.-H., Tang, Y., Yin, H.-Y., & Yu, S.-G. (2014) · Journal of Acupuncture and Tuina Science · doi:10.1007/s11726-014-0773-y
- Authors
- Baloyannis, S. J., Costa, V., & Michmizos, D.
- Affiliations
- Aristotle University of Thessaloniki (GR)
- ORCID
- Costa, Vassiliki
- Venue
- American Journal of Alzheimer's Disease & Other Dementias®
- Publisher
- SAGE Publications
- Published
- 2004-03
- Volume
- 19
- Issue
- 2
- Pages
- 89-93
- ISSN
- 0888-4897 (ISSN-L)
- 1533-3175
- 1938-2731
- PMC
- PMC10834007
- OpenAlex
- W1994060945
- Cited by
- 206
- References
- 0
- Citations by year
- 2025: 6 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 14 · 2020: 15 · 2019: 12 · 2018: 13 · 2017: 16 · 2016: 17 · 2015: 9 · 2014: 14 · 2013: 10 · 2012: 12
- FWCI
- 3.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Alzheimer s Disease & Other Dementias® (publishedVersion)
- PubMed Central (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
- Alzheimer's disease, mitochondrial morphology, mitochondrial cristae, neuronal ultrastructure, thalamus, red nucleus, globus pallidus, dendritic spines, oxidative damage, subcortical neurons, energy deficiency
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Humans, Male, Mass Screening, Middle Aged, Mitochondria, Neuropsychological Tests
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