Table 2.

Therapeutic approaches targeting cGAS-STING signaling pathway for central nervous system (CNS) diseases.

CNS diseases	Therapeutic approaches	Mechanism	Type of study	References
IS	A151	Inhibits cGAS	In vivo and in vitro model	Li et al. (2020)
	HDAC3 inhibitors	Inhibits cGAS	In vivo and in vitro models	Liao et al. (2020)
	VIN	Inhibits cGAS	In vivo and in vitro models	Shi et al. (2022)
	C-176	Inhibits STING	In vivo and in vitro models	Kong et al. (2022)
AD	NR	Stimulates mitophagy, reduce cytoplasmic DNA	In vivo and in vitro models	Hou et al. (2021)
PD	Inhibits Drp1	Decreases mitochondrial fission, reduce mtDNA	In vivo and in vitro models	Weindel et al. (2020)
HD	Melatonin	Decreases mitochondrial ROS injury, reduce mtDNA	In vivo and in vitro models	Jauhari et al. (2020)
MS	GCV	Activates the IFN-I response in a STING-dependent manner and reduces neuroinflammation	In vitro models	Mathur et al. (2017)
A-T	H-151	Inhibits STING	In vitro models	Aguado et al. (2021)
	Aspirin	Inhibits cGAS through acetylation	In vitro models	Aguado et al. (2021)
AGS	EGCG	Inhibits G3BP1 to suppresses the activation of cGAS	In vivo and in vitro models	Liu et al. (2019)
	Aspirin	Acetylates cGAS to inhibit cGAS-mediated immune responses	In vivo and in vitro models	Dai et al. (2019)

A151, synthetic oligodeoxynucleotide; cGAS, cyclic GMP–AMP synthase; HDAC3, histone deacetylase 3; VIN, versatile immunosuppressive nanoparticle; C-176, a small molecule inhibitor of STING; STING, stimulator of interferon genes; AD, Alzheimer’s disease; NR, nicotinamide riboside; PD, Parkinson’s disease; Drp1, dynamin-related protein; mtDNA, mitochondrial DNA; HD, Huntington’s disease; MS, multiple sclerosis; GCV, Ganciclovir; IFN-I, type I interferon; A-T, ataxia–telangiectasia; H-151, a small molecule inhibitor of STING; AGS, Aicardi-Goutières syndrome; EGCG, epigallocatechin gallate; G3BP1, GTPase-activating protein SH3 domain–binding protein 1.