Under inflammatory stimulation, lncRNA-17A can direct G-protein-coupled receptor 51 (GPR51) splicing to produce isoform variant B of the B-type receptor for the neurotransmitter g-aminobutyric acid (GABA; GABAB receptor). Because only the canonical variant, isoform A, contains the complete C-terminal portion needed to interact with GABAB R1 to generate a functional heterodimeric receptor, this alternative splicing causes the synthesis of a non-functional GABAB receptor. In addition, the overexpression of 17A causes an overproduction of Aβ.28