Neuroprotective signaling by hydrogen sulfide and its dysregulation in Alzheimer's disease

Curr Opin Chem Biol. 2024 Oct:82:102511. doi: 10.1016/j.cbpa.2024.102511. Epub 2024 Aug 13.

Abstract

The ancient messenger molecule hydrogen sulfide (H2S) modulates myriad signaling cascades and has been conserved across evolutionary boundaries. Although traditionally known as an environmental toxin, H2S is also synthesized endogenously to exert modulatory and homeostatic effects in a broad array of physiologic functions. Notably, H2S levels are tightly physiologically regulated, as both its excess and paucity can be toxic. Accumulating evidence has revealed pivotal roles for H2S in neuroprotection and normal cognitive function, and H2S homeostasis is dysregulated in neurodegenerative conditions. Here, we review the normal neuroprotective roles of H2S that go awry in Alzheimer's disease, the most common form of neurodegenerative disease.

Keywords: Alzheimer's disease; Cysteine; Hydrogen sulfide; Sulfhydration; Tau.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / therapy
  • Amyloid / metabolism
  • Animals
  • Brain / metabolism
  • Homeostasis
  • Hydrogen Sulfide* / metabolism
  • Neuroprotection
  • Signal Transduction*
  • tau Proteins / metabolism

Substances

  • Hydrogen Sulfide
  • tau Proteins
  • Amyloid