Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology
Open accessAbstract
Mitochondria are uniquely poised to play a pivotal role in neuronal cell survival or death because they are regulators of both energy metabolism and cell death pathways. Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer's disease. This review discusses evidence indicating that mitochondrial dysfunction has an early and preponderant role in Alzheimer's disease. Furthermore, the link between mitochondrial dysfunction and autophagy in Alzheimer's disease is also discussed. As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy, neurons progressively accumulate lipofuscin that could exacerbate neuronal dysfunction. Since autophagy is the major pathway involved in the degradation of protein aggregates and defective organelles, an intense interest in developing autophagy-related therapies is growing among the scientific community. The final part of this review is devoted to discuss autophagy as a potential target of therapeutic interventions in Alzheimer's disease pathophysiology.
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Metal ions specifically zinc and copper may bind to the Aβ plaque and produce reactive oxygen species (ROS).
“Metal ions specifically zinc and copper may bind to the Aβ plaque and produce ROS.”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [29]
ROS produced brings about oxidative change in the Aβ peptide itself making its removal difficult and also causes lipid and protein oxidation of the cell membrane making it permeable and hence susceptible to degeneration.
“ROS thus produced brings about oxidative change in the Aβ peptide itself making its removal difficult and also cause lipid and protein oxidation of the cell membrane making it permeable and hence susceptible to degeneration [24, 29, 30].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [29]
Aβ peptides can induce ROS production from mitochondria, leading to release of cytochrome c and apoptosis-inducing factor, thereby driving mitochondrial dysfunction, cell apoptosis, and neuronal loss.
“Aβ peptides can induce ROS production from mitochondria, leading to release of cytochrome c and apoptosis-inducing factor, thereby driving mitochondrial dysfunction, cell apoptosis and neuronal loss [97, 100].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [100]
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“ROS thus produced brings about oxidative change in the Aβ peptide itself making its removal difficult and also cause lipid and protein oxidation of the cell membrane making it permeable and hence susceptible to degeneration [24, 29, 30].”
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- Authors
- Moreira, P. I., Carvalho, C., Zhu, X., Smith, M. A., & Perry, G.
- Affiliations
- Centro de Neurociências e Biologia Celular (PT)
- Case Western Reserve University (US)
- The University of Texas at San Antonio (US)
- Corresponding author
- Perry, George
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 1802
- Issue
- 1
- Pages
- 2-10
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2010484888
- Cited by
- 734
- References
- 78
- Citations by year
- 2026: 17 · 2025: 32 · 2024: 40 · 2023: 69 · 2022: 61 · 2021: 62 · 2020: 78 · 2019: 75 · 2018: 71 · 2017: 48 · 2016: 59 · 2015: 29 · 2014: 19 · 2013: 9 · 2012: 21
- FWCI
- 2.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- 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 › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, Alzheimer's disease, oxidative damage, autophagy, lipofuscin, protein aggregates, neuronal cell death, energy metabolism
- MeSH terms
- Alzheimer Disease, Animals, Autophagy, Brain, Humans, Mitochondria, Models, Biological
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