Our results suggest that down-regulation of miR-34b and miR-34c in the brain, as well as an SNP in the 3'-UTR of α-syn can increase α-syn expression, possibly contributing to PD pathogenesis.
For example, miR-133b is deficient in the PD midbrain as well as in mouse models, and miR-34b/34c are decreased in several affected brain regions in PD and incidental Lewy body disease.
We propose that early deregulation of miR-34b/c in PD triggers downstream transcriptome alterations underlying mitochondrial dysfunction and oxidative stress, which ultimately compromise cell viability.