Mini Review - (2024) Volume 13, Issue 1
Received: 02-Jan-2024, Manuscript No. MBL-24-131583;
Editor assigned: 04-Jan-2024, Pre QC No. P-131583;
Reviewed: 14-Feb-2024, QC No. Q-131583;
Revised: 20-Feb-2024, Manuscript No. R-131583;
Published:
29-Feb-2024
, DOI: 10.37421/2168-9547.2024.13.419
Citation: Cammaroto, Salvatore. “Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases.” Mol Biol 13 (2024): 419.
Copyright: © 2024 Cammaroto S. This is an open-access article distributed under the terms of the creative commons attribution license which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, pose significant challenges to global healthcare systems due to their debilitating nature and lack of effective treatments. Recent research has shed light on the intricate interplay between oxidative stress and inflammatory responses in the pathogenesis of these disorders. This article explores emerging insights into the roles of oxidative stress and inflammation in neurodegeneration, highlighting potential therapeutic targets and strategies for mitigating disease progression.
Neurodegenerative • Diseases • Treatments
Neurodegenerative diseases are characterized by the progressive loss of neurons, leading to cognitive decline, motor dysfunction, and ultimately, significant disability. Alzheimer's Disease (AD), Parkinson's Disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are among the most prevalent neurodegenerative conditions, affecting millions worldwide. While the exact etiology of these disorders remains elusive, growing evidence suggests that oxidative stress and inflammatory processes play pivotal roles in their pathogenesis [1].
Oxidative stress arises from an imbalance between the production of Reactive Oxygen Species (ROS) and the antioxidant defense mechanisms within cells. In the context of neurodegenerative diseases, neurons are particularly vulnerable to oxidative damage due to their high metabolic activity and abundant lipid content. Accumulating evidence implicates oxidative stress as a key contributor to neuronal dysfunction and death in AD, PD, and ALS. In AD, the accumulation of amyloid-beta plaques and hyperphosphorylated tau proteins triggers oxidative damage through multiple mechanisms, including mitochondrial dysfunction, activation of NADPH oxidase, and disruption of calcium homeostasis. Similarly, in PD, the aggregation of alpha-synuclein and impaired mitochondrial function contribute to ROS generation and oxidative stress. In ALS, mutations in Superoxide Dismutase 1 (SOD1) and TAR DNABinding Protein 43 (TDP-43) disrupt cellular redox balance, leading to motor neuron degeneration [2]. In addition to oxidative stress, chronic inflammation is a hallmark feature of neurodegenerative diseases.. Upon activation, microglia release pro-inflammatory cytokines, chemokines, and reactive oxygen species, further exacerbating neuronal damage and promoting disease progression.
In AD, neuroinflammation is characterized by the activation of microglia around Aβ plaques, leading to the release of cytokines such as interleukin- 1β (IL-1β) and Tumor Necrosis Factor-alpha (TNF-α). Similarly, in PD, activated microglia are found in close proximity to dopaminergic neurons in the substantia nigra, contributing to neuroinflammation and neuronal loss. In ALS, microglial activation correlates with disease progression, suggesting a role for neuroinflammation in motor neuron degeneration. Emerging evidence suggests that oxidative stress and inflammation are interconnected processes that fuel neurodegeneration through positive feedback loops. ROS generated under conditions of oxidative stress can activate redox-sensitive signaling pathways, such as nuclear factor-kappa B (NF-κB) and Mitogen-Activated Protein Kinases (MAPKs), leading to the production of pro-inflammatory mediators. Conversely, inflammatory cytokines can induce oxidative stress by promoting the expression of NADPH oxidase and impairing antioxidant defences [3,4].
Targeting oxidative stress and inflammation represents a promising therapeutic approach for neurodegenerative diseases. Antioxidant compounds, such as vitamin E, coenzyme Q10, and resveratrol, have shown potential neuroprotective effects in preclinical studies and clinical trials. Similarly, antiinflammatory agents, including nonsteroidal anti-inflammatory drugs and monoclonal antibodies against pro-inflammatory cytokines, hold promise for mitigating neuroinflammation and disease progression.
Moreover, emerging strategies aimed at modulating microglial function, such as the use of microglial inhibitors or immunomodulatory agents, offer new avenues for therapeutic intervention. Additionally, lifestyle modifications, including regular exercise, dietary interventions, and stress reduction techniques, may help alleviate oxidative stress and inflammation, thereby delaying the onset or progression of neurodegenerative diseases [5,6].
Oxidative stress and inflammatory responses play critical roles in the pathogenesis of neurodegenerative diseases, including AD, PD, and ALS. Understanding the intricate interplay between these processes is essential for the development of effective therapeutic strategies aimed at halting or slowing disease progression. Future research efforts should focus on elucidating the molecular mechanisms underlying oxidative stress and inflammation in neurodegeneration, as well as identifying novel therapeutic targets to combat these devastating disorders. By targeting oxidative stress and inflammation, we may ultimately achieve breakthroughs in the treatment of neurodegenerative diseases and improve the quality of life for millions of patients worldwide.
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Molecular Biology: Open Access received 607 citations as per Google Scholar report