STINGing the brain: S-nitrosylation drives neuroinflammation in Alzheimer's disease.

Andrew A Pieper¹, Emiko Miller², Oleh Khalimonchuk³, Bindu D Paul⁴

¹Department of Psychiatry, Case Western Reserve University, Cleveland, OH 44106, USA; Brain Health Medicines Center, Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA; Geriatric Psychiatry, GRECC, Louis Stokes VA Medical Center, Cleveland, OH 44106, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address: aap143@case.edu.

²Department of Psychiatry, Case Western Reserve University, Cleveland, OH 44106, USA; Brain Health Medicines Center, Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA; Geriatric Psychiatry, GRECC, Louis Stokes VA Medical Center, Cleveland, OH 44106, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106, USA.

³Department of Biochemistry and Nebraska Redox Biology Center, University of Nebraska-Lincoln, Lincoln, NE 68588, USA.

⁴Department of Physiology, Pharmacology & Therapeutics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: bpaul8@jhmi.edu.

PubMed DOI

Abstract

Neuroinflammation is a major secondary driver of Alzheimer's disease (AD). In this issue of Cell Chemical Biology, Carnevale et al.1 demonstrate that S-nitrosylation of the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway sustains pathological neuroinflammation in AD, identifying a promising therapeutic target for this devastating disease.

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