BACE1 antisense RNA (non-protein coding) (BACE1-AS)

BACE1 antisense RNA (BACE1-AS) is a long noncoding RNA transcribed from the opposite strand of the BACE1 gene on chromosome 11q23.3 in humans[1][2]. Functionally, BACE1-AS forms RNA duplexes with BACE1 mRNA, stabilizing it and increasing BACE1 expression as well as amyloid β (Aβ) production through a post-transcriptional feed-forward loop[1][2][5]. In Alzheimer’s disease, both BACE1-AS and BACE1 are upregulated, promoting amyloidogenic processing of amyloid precursor protein and plaque formation[1][2]. Experimental knockdown of BACE1-AS reduces BACE1 expression, lowers Aβ levels, ameliorates senile plaque deposition, and reduces neuronal injury in vitro and in animal models, highlighting therapeutic potential[1][4][5]. BACE1-AS also acts as a competing endogenous RNA, sponging specific microRNAs (e.g., miR-214-3p) that target BACE1 and autophagy genes, thereby contributing to neuronal autophagy and neurotoxicity[4]. BACE1-AS is being explored as a biomarker and putative therapeutic target for Alzheimer’s and possibly other neurodegenerative disorders[1][4][5].

Other names

BACE1-AS1FJ573250NCRNA00177non-protein coding RNA 177BACE1AS

Modulation of BACE1 mRNA stability (by forming RNA duplex). Competes with microRNAs as a ceRNA (e.g., miR-214-3p) to derepress BACE1 expression. Regulation of amyloid β-peptide generation.