An increasing body of evidence suggests that alterations in neurogenesis and oxidative stress are associated with a wide variety of central nervous system (CNS) diseases. The oxidation state of the CNS is the hallmark of brain ageing and associated with many neurodegenerative disorders, including Parkinson’s disease, Alzheimer’s disease, stroke and amyotrophic lateral sclerosis. The CNS is a highly oxidized environment that is particularly vulnerable to oxidative stress due to the brain’s high oxygen consumption rate, abundant lipid content, and the relative paucity of antioxidant enzymes compared with other tissues. Oxidative stress is an altered biochemical response caused by free reactive oxidative species (ROS) radicals in which the excessive oxidation accelerates protein, membrane, and gene instability, and eventually leads to neurodegenerative diseases due to imbalance in homeostasis in the brain microenvironment. Adult hippocampal neurogenesis plays an important role in normal functions of CNS. Alterations in adult hippocampal neurogenesis are associated with a variety of neurodegenerative diseases. Promoting endogenous hippocampal neurogenesis merits significant attention to cure neurodegenerative disease. The adult CNS harbors two regions of persistent lifelong neurogenesis: the subventricular zone and the dentate gyrus. These regions contain populations of quiescent neural stem cells (NSCs) that generate mature progeny via rapidly dividing progenitor cells. NSCs support adult neurogenesis in nervous system during injuries, and differentiate into neurons, astrocytes or oligodendrocytes. Impaired neurogenesis and inadequate induction of neurogenesis are the main obstacles in treatment of neurodegenerative diseases.

Protection of neural cells from oxidative damages and supporting neurogenesis are promising strategies to treat neurodegenerative diseases. However, oxidative stress leads to free radical attack on NSCs, which contributes to protein misfolding, glia cell activation, mitochondrial dysfunction, impairment of DNA repair system and subsequently cellular death. The mechanism for stress to affects the function of neural stem or progenitor cells in the dentate gyrus of hippocampus is not clear. Therefore, a better understanding of adult hippocampal neurogenesis at oxidative stress can facilitate a more successful prevention for neurodegenerative disease.

In this Special Issue, we welcome high-quality original research and review articles on the mechanisms of oxidative stress affecting neurogenesis and finally leading to neurodegenerative disease.

Potential topics include but are not limited to the following:

• Neural mechanism of oxidative stress and neurogenesis with damage or improving astrocyte function property
• Neural mechanisms for oxidative stress induced astrocytic impairment in neurodegenerative diseases
• Neural mechanism for age-related oxidative stress affecting astrocytic function and neurogenesis
• Molecular mechanism of drug medicine, which is involved in regulation of oxidative stress and astrocytic reaction in the context of neurodegenerative diseases
• Methodology of isolation/testing/screening strategy for the discovery of novel anti-brain aging medicinal agents.
• Future prospectives for research on the oxidative stress affecting neurogenesis and its relationship with neurodegenerative disorders and drug medicines of anti-aging research.