Molecular Mechanisms of Thiol-Based Redox Homeostasis and Signaling in the Brain

It is becoming increasingly clear that thiols play a central role in maintenance of redox homeostasis in living systems. Thiols undergo a myriad of redox reactions which contribute to a rich array of signaling molecules. Thus, cells are endowed with a multitude of sulfur containing molecules such as cysteine, homocysteine, lanthionine and taurine, peptides such as glutathione and gaseous signaling molecules such as hydrogen sulfide. Cysteine residues on proteins undergo the maximum number of posttranslational modifications, which include but is not limited to nitrosylation, persulfidation, sumoylation and palmitoylation. These modifications play vital roles in cellular physiology and fine tune responses to stress stimuli as well as normal cellular processes. Redox signaling is especially important in the brain, which is metabolically highly active. Disruption of redox signaling is a hallmark of several neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis and Ataxias. Emerging evidence suggests that redox imbalances contribute to disease progression and pathophysiology of these diseases. Redox signaling in the brain has been relatively less studies as compared to that in peripheral tissues.

In this Research Topic, we bring together, a collection of articles that highlight the signal transduction cascades operating in the brain, their derangement in neurodegeneration and methods to quantify and detect these processes as well as points of therapeutic intervention.