Alpha-synuclein (alpha-SYN) is one of the key contributors in Parkinson's disease (PD) pathogenesis. Despite the fact that increased alpha-SYN levels are considered one of the key contributors in developing PD, the molecular mechanisms underlying the regulation of alpha-SYN still needs to be elucidated. Since the 3' untranslated regions (3'UTRs) of messenger RNAs (mRNAs) have important roles in translation, localization, and stability of mRNAs through RNA binding proteins (RBPs) and microRNAs (miRNAs), it is important to identify the exact length of 3'UTRs of transcripts in order to understand the precise regulation of gene expression. Currently annotated human alpha-SYN mRNA has a relatively long 3'UTR (2529 nucleotides [nt]) with several isoforms. RNA-sequencing and epigenomics data have suggested, however, the possible existence of even longer transcripts which extend beyond the annotated alpha-SYN 3'UTR sequence. Here, we have discovered the novel extended form of alpha-SYN 3'UTR (3775 nt) in the substantia nigra of human postmortem brain samples, induced pluripotent stem cell (iPSC)-derived dopaminergic neurons, and other human neuronal cell lines. Interestingly, the longer variant reduced alpha-SYN translation. The extended alpha-SYN 3'UTR was significantly lower in iPSC-derived dopaminergic neurons from sporadic PD patients than controls. On the other hand, alpha-SYN protein levels were much higher in PD cases, showing the strong negative correlation with the extended 3'UTR. These suggest that dysregulation of the extended alpha-SYN 3'UTR might contribute to the pathogenesis of PD.