ELAVL4 (HuD) is a neuron-enriched RNA-binding protein that post-transcriptionally regulates mRNA stability, alternative splicing, and translation 1. The protein binds AU-rich elements (AREs) in the 3' untranslated regions (3'UTR) of target mRNAs including GAP43, VEGF, and ACHE, decreasing mRNA deadenylation and protecting transcripts from decay 23. ELAVL4 plays a critical role in neuron-specific RNA processing, promoting neural progenitor differentiation and contributing to learning, memory, neurite outgrowth, and dendritic development 45. ELAVL4 dysfunction is implicated in multiple neurodegenerative diseases. In Alzheimer's disease, ELAVL4 knockout increases pathological APP isoforms and phosphorylated tau, while overexpression reduces extracellular amyloid-beta levels 6. In amyotrophic lateral sclerosis (ALS), FUS mutations increase HuD levels, causing overstabilization of axonal growth transcripts NRN1 and GAP43 7, and HuD overexpression impairs neuromuscular junctions and induces motoneuron apoptosis 8. In frontotemporal dementia, ELAVL4 upregulation precedes glutamatergic neuronal loss 9. Additionally, ELAVL4 regulates neuronal dsRNA levels through 3'UTR length control, maintaining antiviral immunity while preventing pathological neuroinflammation 10. Beyond neurology, ELAVL4 stabilizes oncogenic lncRNAs in small cell lung cancer 11. These findings establish ELAVL4 as a critical neuronal RBP with therapeutic potential across multiple disease contexts.