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Mitochondrial alterations in Alzheimer's disease
Abstract
Morphological alterations of mitochondria may be related to metabolic and energy deficiency in neurons in Alzheimer's disease and other neurodegenerative disorders. Mitochondrial dysfunction is also a hallmark of beta peptide induced neuronal toxicity in Alzheimer's disease. A general change in glucose utilization, increased oxidative stress, and Ca;{2+} deregulation are additional metabolic defects in the AD brain that may also be associated with defective mitochondrial function the result is a cycle of increased mitochondrial dysfunction causing increased oxidative damage until the cellular energy supply falls below the threshold for cellular survival. In a series of studies on the morphological and morphometric estimation of mitochondria in Alzheimer's disease, by electron microscopy we noticed substantial morphological and morphometric changes in the neurons of the hippocampus, the acoustic cortex, the frontal cortex, the cerebellar cortex, the climbing fibers, the thalamus, the globus pallidus, the red nucleus and the locus coeruleus. The morphological alterations consisted of considerable 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 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, though they were prominent in neurons, which demonstrated fragmentation of the cisternae of the Golgi apparatus. Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease. The relationship between the site and extent of mitochondrial abnormalities and the synaptic alterations suggests an intimate and early association between these features in Alzheimer's disease.
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“Most studies report the number of intact, normal appearing mitochondria declines [111, 138].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [138]
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“ARC Journal of Neuroscience Page | 2 event in the progression of AD [13, 14].”
BackgroundYeast as a Model for Studying Aβ Aggregation, Toxicity and Clearance
Bharadwaj, P. (2011) · Australasian Journal of Paramedicine · Cited by 1
Moll, C. W. I., Lindtner, R. A., Vogel, G. F., et al. (2016) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/046300 · Cited by 1
“In contrast, changes in mitochondrial size and distribution have been 358 reported for brain and peripheral cells of patients with bipolar disorders [16], in the number 359 [17] and appearance of mitochondria of cancer cells [18], and in the cristae morphology and 360 size of mitochondria of neurons from patients with…”
BackgroundChatterjee, A., Alvarez, B., Sharma, R. U., et al. (2025) · medRxiv · doi:10.1101/2025.09.25.25336251 · Cited by 1
“3 Mitochondrial dysfunction plays a prominent role in two of the most common neurodegenerative diseases - Alzheimer’s disease (AD) and Parkinson’s disease (PD) 4,5 .”
Bezine, M. (2017) · theses.fr (ABES) · doi:10.70675/a634c389z7b07z4830zb56dzbf7b53a56944 · Cited by 1
Liu, M. (2011) · UCL Discovery (University College London)
Role of Mitochondria in Alzheimer ́s Disease
Ortiz, G. G., Pacheco-Moisés, F. P., García-Trejo, J. D. J., Rocio, E., Miguel, A., Jose, A., Irma, E., Arias‐Merino, E. D., & de la Ros, A. C. (2011) · InTech eBooks · doi:10.5772/16713
“…cristae (Hirai et al., 2001), the accumulation of osmiophylic material and significant decreases in mitochondrial size are found www.intechopen.com Alzheimer’s Disease Pathogenesis-Core Concepts, Shifting Paradigms and Therapeutic Targets 300 predominantly in neurons (Baloyannis, 2006).”
BackgroundNakamura, T., & Lipton, S. A. (2011) · Wiley eBooks · doi:10.1002/9781118063903.ch2
Stimulating Neuroprotective and Regenerative Mechanisms in Alzheimer Disease
Lilja, A. M. (2013) · Zenodo (CERN European Organization for Nuclear Research) · doi:10.5281/zenodo.8515
“Aβ-mediated activation of microglia stimulates the production of reactive oxygen species, which in turn leads to oxidative stress and mitochondrial dysfunction (Baloyannis et al., 2004; Butterfield et al., 2001; Sas et al., 2007).”
BackgroundMitochondria-targeted amyloid: Relevance to neurotoxicity and Alzheimer's disease
Tillement, L. (2011) · DigitalGeorgetown (Georgetown University Library)
Genetic and lifestyle influences on memory, brain structure, and dementia
Ferencz, B. (2017) · Figshare
Alternation of Mitochondrial and Golgi Apparatus in Neurodegenerative Disorders
Sharma, S., Kaur, P., Gupta, S., & Sharma, S. (2018) · Advances in medical diagnosis, treatment, and care (AMDTC) book series · doi:10.4018/978-1-5225-5282-6.ch005
“…and GA on the dysfunction of neurons that result in various NDs. Mitochondrial play an important role in Ca2+ homeostasis, ATP generation, ROS formation, and even apoptosis etc. and any dysfunction in these processes results in the dysfunction of neurons in a large number of NDs (Baloyannis, 2006).”
BackgroundMitochondria 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
Mitochondrial Aspects of Neuronal Pathology in Triple-Transgenic Alzheimer’s Disease Mice
Cavendish, J. Z. (2019) · The Research Repository @ WVU (West Virginia University) · doi:10.33915/etd.4024
“The reduction in mitochondrial volume and increase in mitochondrial sphericity in CA1 supports previous data showing hippocampal mitochondrial structural abnormalities in the hippocampus of AD patients and 3xTg-AD mice [76, 78].”
BackgroundResultInfluential
Metadata
- Authors
- Baloyannis, S. J.
- Affiliations
- Department of Neurology, Aristotelian University, Thessaloniki 540 06, Greece
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2006-07-14
- Volume
- 9
- Issue
- 2
- Pages
- 119-126
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2120143950
- Cited by
- 318
- References
- 0
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 8 · 2023: 11 · 2022: 14 · 2021: 28 · 2020: 28 · 2019: 16 · 2018: 18 · 2017: 21 · 2016: 21 · 2015: 13 · 2014: 11 · 2013: 11 · 2012: 20
- FWCI
- 6.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- 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, mitochondrial dysfunction
- MeSH terms
- Alzheimer Disease, Animals, Energy Metabolism, Homeostasis, Humans, Mitochondria, Oxidative Stress
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