Abstract: Most neurological diseases are associated with a tissue injury that is detected by the innate immune response (IIR), leading to an inflammatory component. The IIR is activated through conserved Pattern Recognition Receptors, including membrane bound Toll like receptors (TLRs), intracellular nucleotide-binding oligomerization domain like receptors and the receptors for advanced glycation end-products (Amor et al., 2010; Heppnerrt et al., 2015). These receptors detect highly conserved structural motifs of damaged or stressed tissues (danger-associated molecular patterns (DAMP)). Cytosolic receptors of nucleic acids, such as cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) and melanoma differentiation associated gene 5 (MDA-5) can also trigger IIR activation leading to interferon (IFN) and IFN stimulated gene (ISG) expression through DNA/RNA sensing signaling pathways (Yang and Li, 2020). Once bound to their cognate receptor, the recognition complexes migrate into the nucleus and initiate different signaling cascades that eventually lead to central nervous system (CNS) inflammation.