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Oxidative toxicity in diabetes and Alzheimer's disease: mechanisms behind ROS/ RNS generation
Waqar Ahmad1, Bushra Ijaz2, Khadija Shabbiri3
1School of Biological Sciences, University of Queensland, Brisbane, 4072, Australia. waqarchemist@hotmail.com.
Abstract:
Reactive oxidative species (ROS) toxicity remains an undisputed cause and link between Alzheimer's disease (AD) and Type-2 Diabetes Mellitus (T2DM). Patients with both AD and T2DM have damaged, oxidized DNA, RNA, protein and lipid products that can be used as possible disease progression markers. Although the oxidative stress has been anticipated as a main cause in promoting both AD and T2DM, multiple pathways could be involved in ROS production. The focus of this review is to summarize the mechanisms involved in ROS production and their possible association with AD and T2DM pathogenesis and progression. We have also highlighted the role of current treatments that can be linked with reduced oxidative stress and damage in AD and T2DM.
Insights
Reactive oxidative species (ROS) cause toxicity linked to Alzheimer's disease (AD) and Type-2 Diabetes Mellitus (T2DM). This review explores ROS production mechanisms and their role in AD and T2DM, including treatment impacts.
Area of Science:
- Neuroscience
- Endocrinology
- Biochemistry
Background:
- Reactive oxidative species (ROS) toxicity is a key factor linking Alzheimer's disease (AD) and Type-2 Diabetes Mellitus (T2DM).
- Oxidative damage to DNA, RNA, proteins, and lipids in patients with both AD and T2DM can serve as disease progression markers.
- While oxidative stress is implicated, multiple pathways contribute to ROS generation in these conditions.
Purpose of the Study:
- To review the mechanisms of ROS production in the context of AD and T2DM.
- To elucidate the association between ROS production pathways and the pathogenesis and progression of AD and T2DM.
- To highlight current therapeutic strategies that may mitigate oxidative stress and damage in these comorbid diseases.
Main Methods:
- Literature review focusing on mechanisms of ROS production.
- Analysis of studies linking ROS pathways to AD and T2DM pathogenesis.
- Evaluation of treatment effects on oxidative stress markers in AD and T2DM.
Main Results:
- Multiple pathways contribute to ROS generation, exacerbating oxidative stress in AD and T2DM.
- Oxidative damage markers correlate with disease progression in comorbid AD and T2DM.
- Certain treatments show potential in reducing oxidative stress and associated damage.
Conclusions:
- Understanding ROS production mechanisms is crucial for managing comorbid AD and T2DM.
- Targeting ROS pathways may offer novel therapeutic avenues for both diseases.
- Further research is needed to fully elucidate the therapeutic potential of antioxidant strategies.
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