Brain-derived neurotrophic factor antisense RNA (BDNF-AS)

Brain-derived neurotrophic factor antisense RNA (BDNF-AS) is a long non-coding RNA transcribed from the opposite strand of the BDNF gene, primarily expressed in the central nervous system[1]. It functions as a natural antisense transcript, forming double-stranded RNA duplexes with BDNF mRNA, and acts as a key negative regulator of BDNF transcription through recruitment of chromatin-modifying enzymes such as EZH2, which promotes repressive histone methylation (H3K27me3) at the BDNF promoter[2][3][4]. Elevated levels of BDNF-AS suppress BDNF expression, increase neuronal apoptosis, and decrease cell viability, while inhibition leads to increased BDNF levels, enhanced neuronal differentiation, and survival. BDNF-AS is implicated in neurodegenerative diseases such as Alzheimer’s and Huntington’s disease, as well as psychiatric disorders related to synaptic plasticity[4]. The main therapeutic strategy under investigation involves antisense oligonucleotides directed at BDNF-AS to upregulate BDNF, representing a promising avenue for neuroprotection and disease modification, albeit with notable challenges related to specificity and epigenetic safety[2][4].

Other names

BT2ABT2BBT2CBT2DNCRNA00049BDNF-AS1BDNFASnon-protein coding RNA 49BDNF antisense RNA 1 (non-protein coding)ANTI-BDNFBDNFOSbrain-derived neurotrophic factor opposite strandBDNF antisense RNA (non-protein coding)BDNF opposite strand (non-protein coding)

ASOs/AntagoNATs bind BDNF-AS RNA, promoting its degradation or blocking its function. Knockdown/inhibition of BDNF-AS increases BDNF mRNA and protein levels, thereby enhancing neuronal differentiation and survival