Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and frontotemporal dementia are among the most pressing problems of developed societies with ageing populations. Although in the central nervous system (CNS) neurons carry out essential functions such as signal transmission and network integration, glial cells are fundamental for homoeostasis, defence, and regeneration. In the CNS, glial cells are generally subdivided into astrocytes, oligodendrocytes, NG2-glia, and microglia. Astrocytes sustain neurotransmission by supplying neurons with neurotransmitter precursors and regulate metabolic homeostasis through synthesising glycogen and supplying neurons with energy substrates. Oligodendrocytes enwrap axons with the myelin sheath and provide them with local metabolic, structural, and homeostatic support. NG2-glia mostly maintain a pool of myelinating cells throughout life. Microglial cells contribute to a wide array of functions in neural development and in neuronal plasticity through secreting factors that affect synaptic transmission. Moreover, the loss of neuroglial function and glial reactivity may contribute to the ageing of the brain and to neurodegenerative diseases.

Oxidative stress, environmental factors, ageing, protein dysfunction, heavy metal pollution, drug abuse, alcoholism, and virus invasion are all common risk factors for neural function deficits and neurodegenerative diseases. Glial morphology and function can be regulated through the stimulation of these risk modulators. Both reactivity and atrophic changes of astrocytes are observed in AD model mice and in human patients, while the pathological remodelling of astrocytes affects their homeostatic and neuroprotective functions. Moreover, oxidative stress can lead to astrocyte defects, whereas several factors, for example, environmental toxins interacting with astrocytes, may contribute to the emergence or enhancement of oxidative stress in age-related neurodegenerative diseases. Oxidative stress is a widespread pathological phenomenon that damages cell components such as DNA, lipids, and proteins. Developing oxidative stress indicates that other endogenous antioxidant defence systems are insufficient or that free radicals and oxidants are being overproduced. Recently, many studies have demonstrated that the progression of age-related neurodegenerative disorders is associated with decreased antioxidant defence and increased oxidative damage to the homeostatic and defensive pathways of neuroglia. In addition, oxidative stress may instigate neuroinflammation, which is fundamentally regulated by various reactive changes in glial cells. These pathological changes are an important component of the pathogenesis of neurodegenerative diseases, with astrocytes and microglia being a target for therapies aimed at the prevention, retardation, and curing of neurodegenerative disorders. However, the related mechanisms of glial neuropathology or neuroprotection in associated neurodegenerative diseases still require further investigation.

In this Special Issue, we aim at promoting research into the functions of glial cells in neurodegenerative diseases, to investigate the mechanisms of glial neuropathology in neurodegenerative diseases, and to explore that role that oxidative stress plays in relation to glial cells, including the effects of decreased antioxidant defence and increased oxidative damage on neuroglia. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• Oxidative stress-related glial pathological mechanisms of neurodegenerative diseases
• Glial cell-related mechanisms of neurodegenerative diseases induced by environmental risk factors, such as metal elements, air pollutants, and photochemical reactions
• The effects of oxidative stress on glial cells in neurodegenerative diseases induced by drug abuse, alcohol overdose, and cytotoxicity
• Oxidative stress-related pharmacological targets of glial cells in neurodegenerative diseases
• The role of glial cells in oxidative and antioxidant defence systems
• Glia-related mechanisms of oxidative stress induced by damage to cell components
• Glia-related mechanisms of oxidative stress induced by chronic or acute infection
• Mechanisms of oxidative stress induced by abnormal glucose regulation in glial cells
• The effects of glial oxidative stress in neurodegenerative diseases induced by mood disorders
• Glia-related mechanisms of neurodegenerative diseases induced by oxidative stress, such as the abnormal catalytic decomposition of superoxide dismutase, catalase, and glutathione peroxidase
• The role of glial cells in oxidative stress caused by smoking, drinking, excessive exercise, drug abuse, and excessive ultraviolet radiation
• Glia-related mechanisms of oxidative stress induced by insufficient nutrients such as selenium, vitamin E, vitamin A, or other key antioxidants