Neurodegenerative disorders are a heterogeneous group of diseases in which there is slow and progressive loss of structure and function of neurons. Alzheimer’s, Parkinson’s, Spinal muscular atrophy, Spinocerebellar ataxia, Motor neurone diseases, Huntington's disease, and Prion disease are some of common neurodegenerative disorders. Neurons involved in these diseases belong to both the central and peripheral nervous system. There are several mechanisms of pathogenesis involved in the development of neurodegenerative disorders. External and internal stressors lead to activation of neuroglial cells which contributes to the disruption of normal nervous functions and stimulates the process of apoptosis in the neuronal cells.

Redox balance plays a key role in the homeostatic regulation of physiological and pathological functions. Increasing evidences have indicated the importance of redox homeostasis in the maintenance of nervous system function. When an overload of free radicals cannot be eliminated, the accumulation induces a phenomenon known as “oxidative stress”. The accumulation of reactive oxygen species (ROS) causes damage to mitochondrial DNA, disturbing the integrity of energy cycle, which is essential for neurological development and function. Inflammation in the neuronal tissues occurs due to accumulation of ROS, which stimulates the synthesis of cytokines and other inflammatory mediators by activating the inflammasome pathway. The nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome is one of the most studied inflammasomes in neurodegenerative diseases. Mitochondrial and lysosomal damage in the cells also involves the activation of NLRP3. This triggers the transformation of procaspase-1 to caspase-1, catalyzing the formation of the mature IL-1β and IL-18, which activates the microglia cells and leads to apoptosis in the neuronal cells. Currently, various therapeutic pathways take advantage of the inhibition of the NLRP3 inflammasome. In Alzheimer’s disease, inhibition of NLRP3 can significantly inhibit amyloidosis and neuropathy and ameliorate cognitive impairment. Thus, antioxidant therapy represents a promising avenue for the treatment of these diseases. However, the complexity and variability of redox biology have largely prevented the investigations of the mechanisms of and therapeutic strategies for neurological diseases.

This Special Issue invites original papers and reviews concerning oxidative stress and redox mechanisms in the activation of inflammatory pathway in the development of neurological/neurodegenerative disorders. Articles that address the novel redox markers, inflammatory pathway, and approaches for diagnosis and treatment are encouraged. We are particularly interested in studies targeting redox signaling pathways for the treatment and prevention of neurodegenerative disorders using animals or cellular models by targeting the inflammatory cascade.

Potential topics include but are not limited to the following:

• The role of oxidative stress in neurodegeneration
• The involvement of inflammasomes in neurodegeneration
• Strategies to prevent/treat redox-related neurological disorders
• Effects of ROS and inflammasomes in cellular death and apoptosis
• Novel antioxidant agents against neuronal death
• The role of redox balance in neurodevelopment, neurogenesis, and neuro-regeneration
• The alterations of redox biology in the interactions between glia and neurons