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Author Spotlight: Decoding Mitochondrial Aging
Published on: June 30, 2023
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Mitochondria in Alzheimer's Disease Pathogenesis
Allison B Reiss1, Shelly Gulkarov1, Benna Jacob1
1Department of Medicine and Biomedical Research Institute, NYU Grossman Long Island School of Medicine, Mineola, NY 11501, USA.
Life (Basel, Switzerland)
|February 24, 2024
Summary
Mitochondrial dysfunction significantly contributes to Alzheimer's disease (AD) pathogenesis by impairing energy production and increasing oxidative stress. Restoring mitochondrial health presents a promising therapeutic avenue for treating this neurodegenerative disorder.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder causing dementia.
- AD pathology involves amyloid-beta plaques and tau tangles.
- Mitochondrial dysfunction is increasingly recognized as a key factor in AD.
Purpose of the Study:
- To review the multifaceted roles of mitochondrial structure and function abnormalities in Alzheimer's disease.
- To highlight the neurotoxic consequences of mitochondrial dysregulation in AD.
Main Methods:
- Literature review focusing on mitochondrial processes in AD.
- Analysis of cellular bioenergetics and signaling pathways in the context of AD.
- Examination of oxidative stress and energy metabolism disruptions.
Main Results:
- Dysregulated mitochondrial dynamics (fission, fusion, trafficking, mitophagy) impair synaptic activity.
- Excessive mitochondrial fission leads to reduced energy production.
- Impaired electron transport chain and ATP synthesis are neurotoxic.
- Mitochondrial dysfunction exacerbates oxidative stress in the AD brain.
Conclusions:
- Abnormal mitochondrial structure and function are critical contributors to Alzheimer's disease.
- Targeting mitochondrial health may offer a viable therapeutic strategy for AD treatment.
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