Editorial: Redox regulation and signaling in neurodegenerative diseases

The production of reactive oxygen, nitrogen, and sulfur species plays a key role in intra- and intercellular signal transduction (Ray et al., 2012; Angelova and Abramov, 2018; Nissanka and Moraes, 2018). As second messengers, these molecules are enzymatically produced and they are essential for regulation of posttranslational modifications of proteins, biochemical pathways, and cellular functions (Dröge, 2002). The identification and characterization of redox molecules, redox-regulated pathways, and functions in different brain areas has also shed light on the origin of oxidative distress and neurodegeneration in the central nervous system (Patten et al., 2010). In fact, there is increasing evidence suggesting that redox changes occur in the early stages of neurodegenerative diseases such as Amyotrophic lateral sclerosis, Alzheimer's (AD), Huntington's, and Parkinson's disease (PD). However, different brain areas are affected and the biochemical and pathophysiological characteristics they display are distinct from one another (Patten et al., 2010; Angelova and Abramov, 2018). To this day, the causes that give rise to the hallmarks and symptoms of many neurodegenerative pathologies remain mostly elusive, however, oxidative distress has been linked to neurodegeneration and -inflammation. We believe that it is important to better understand redox biology on a molecular, biochemical, and cellular level and also, to translate this knowledge to the clinics.