Redox regulation plays a central role in signal transduction processes operating in the brain. Aberrant redox signaling is a hallmark of several neurodegenerative diseases such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis and various Ataxias. It is becoming increasingly clear that redox imbalance contributes to disease progression and pathophysiology of these diseases. My laboratory studies the molecular mechanisms underlying redox homeostasis in the brain with a focus on signaling mediated by gaseous messenger molecules such as hydrogen sulfide (H₂S) and nitric oxide (NO). H₂S and NO signal via post-translational modifications, on reactive cysteine residues, termed persulfidation/sulfhydration and nitrosylation respectively. We also study signaling mediated by redox active small molecules (bilirubin, cysteine, cysteamine, NAD⁺ and glutathione) and associated enzymes. Most recently we have been studying redox signaling in myalgic encephalomyelitis/chronic fatigue syndrome and COVID-19. Using cell culture, mouse models and patient samples, we have shown that modulating sulfhydration and nitrosylation networks have therapeutic benefits. These studies have yielded important clues that may be harnessed to develop novel therapeutics that delay, halt, reverse or better still, prevent neurodegeneration.