Version 1
: Received: 16 August 2024 / Approved: 19 August 2024 / Online: 19 August 2024 (16:45:14 CEST)
How to cite:
ALKHALIFA, A.; Alkhalifa, O.; Durdanovic, I.; R. Ibrahim, D. Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease: Insights into Pathophysiology and Treatment. Preprints2024, 2024081375. https://doi.org/10.20944/preprints202408.1375.v1
ALKHALIFA, A.; Alkhalifa, O.; Durdanovic, I.; R. Ibrahim, D. Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease: Insights into Pathophysiology and Treatment. Preprints 2024, 2024081375. https://doi.org/10.20944/preprints202408.1375.v1
ALKHALIFA, A.; Alkhalifa, O.; Durdanovic, I.; R. Ibrahim, D. Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease: Insights into Pathophysiology and Treatment. Preprints2024, 2024081375. https://doi.org/10.20944/preprints202408.1375.v1
APA Style
ALKHALIFA, A., Alkhalifa, O., Durdanovic, I., & R. Ibrahim, D. (2024). Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease: Insights into Pathophysiology and Treatment. Preprints. https://doi.org/10.20944/preprints202408.1375.v1
Chicago/Turabian Style
ALKHALIFA, A., Iva Durdanovic and Dalia R. Ibrahim. 2024 "Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease: Insights into Pathophysiology and Treatment" Preprints. https://doi.org/10.20944/preprints202408.1375.v1
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and memory loss. Oxidative stress (OS) has emerged as a central element in the pathophysiology of AD, linking various pathological features including amyloid-β (Aβ) plaque formation, tau hyperphosphorylation, and synaptic dysfunction. This review comprehensively examines the role of OS in AD, focusing on the mechanisms of reactive oxygen species (ROS) production, mitochondrial dysfunction, and their impact on neuronal integrity. Additionally, the review highlights recent advances in antioxidant therapy. Elevated ROS levels in the aging brain exacerbate oxidative damage to lipids, proteins, and DNA, contributing to neuronal atrophy and synaptic loss. Mitochondrial dysfunction further amplifies OS, disrupting cellular energy metabolism and promoting neurodegeneration. Despite the strong association between OS and AD, antioxidant therapies have shown inconsistent clinical outcomes. Emerging strategies targeting offer promising avenues for therapeutic intervention. This review highlights the need for a multifaceted approach in understanding and mitigating OS-related damage in AD, aiming to pave the way for more effective treatments and improved patient outcomes.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
