Biology and Medicine

Oxidative Stress in Neurodegeneration: Role of Biomarkers and Exploring Therapeutic Interventions

Xiang Wang^* Department of Neurology, University of Newfoundland, Newfoundland, Canada
^*Correspondence: Xiang Wang, Department of Neurology, University of Newfoundland, Newfoundland, Canada, Email:

Received: 23-Jul-2024, Manuscript No. BLM-24-26983; Editor assigned: 25-Jul-2024, Pre QC No. BLM-24-26983 (PQ); Reviewed: 08-Aug-2024, QC No. BLM-24-26983; Revised: 16-Aug-2024, Manuscript No. BLM-24-26983 (R); Published: 23-Aug-2024, DOI: 10.35248/0974-8369.24.16.718

Description

Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Huntington's disease (HD) and Amyotrophic Lateral Sclerosis (ALS), represent a major challenge in modern medicine due to their progressive nature, complex pathophysiology and lack of curative treatments. One of the key mechanisms implicated in the onset and progression of these disorders is oxidative stress, a condition characterized by an imbalance between the production of Reactive Oxygen Species (ROS) and the antioxidant defenses of the body. Oxidative stress arises when the generation of ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals exceeds the capacity of the body's antioxidant systems, leading to cellular damage. In the brain which is particularly vulnerable to oxidative damage due to its high oxygen consumption and abundant lipid content ROS can inflict damage on proteins, lipids and nucleic acids. This oxidative damage contributes to the dysfunction and death of neurons, a key aspect of neurodegenerative diseases.

In Alzheimer's disease, for example, oxidative stress is closely linked to the formation of amyloid-beta plaques and tau tangles, two key pathological features of the disease. The aggregation of amyloid-beta peptides can generate ROS, which in turn promote further aggregation and neurotoxicity, creating a vicious cycle. Similarly, in Parkinson's disease, oxidative stress is thought to play an essential role in the degeneration of dopaminergic neurons in the substantia nigra, partly due to the oxidative metabolism of dopamine itself. Huntington's disease and amyotrophic lateral sclerosis also exhibit significant oxidative damage in affected neurons. In HD, the mutant huntingtin protein is associated with increased oxidative stress, contributing to the death of striatal neurons. In ALS, mutations in the Superoxide Dismutase 1 (SOD1) gene can lead to impaired antioxidant defense and increased vulnerability to oxidative stress.

The identification of reliable biomarkers for oxidative stress in neurodegenerative diseases is essencial for early diagnosis, monitoring disease progression, and evaluating the efficacy of therapeutic interventions. Biomarkers are measurable indicators of biological processes and oxidative stress, they often reflect the extent of oxidative damage or the status of antioxidant defenses.

Protein carbonyls, which result from the oxidation of amino acid side chains, are also considered biomarkers of oxidative stress and have been found at higher levels in the brains of patients with AD and PD. Additionally glutathione, a major intracellular antioxidant is often depleted in neurodegenerative diseases and its levels can serve as an indirect measure of oxidative stress. Given the central role of oxidative stress in neurodegeneration, therapeutic strategies aimed at reducing oxidative damage hold significant potential. Antioxidants, compounds that neutralize ROS, are a primary focus of these interventions. Vitamin E, a lipid-soluble antioxidant has been studied extensively for its neuroprotective effects. Some clinical trials have shown that vitamin E supplementation can slow the progression of Alzheimer's disease, though results have been mixed and further research is needed. Finally, mitochondria-targeted therapies aim to reduce oxidative stress at its source. By improving mitochondrial function and reducing the production of ROS, these therapies hold promise for protecting neurons from oxidative damage.

Oxidative stress plays an essential role in the pathogenesis of neurodegenerative diseases, contributing to neuronal damage and disease progression. Identifying reliable biomarkers of oxidative stress is essential for early diagnosis and monitoring therapeutic efficacy. While antioxidant therapies offer hope for reducing oxidative damage, challenges remain in translating these interventions into effective treatments. Continued research into the mechanisms of oxidative stress and the development of targeted therapies is essential for advancing the treatment of neurodegenerative diseases and improving outcomes for patients.