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Autosomal dominant mutations in the gene encoding α-synuclein (<i>SNCA</i>) were the first to be linked with hereditary Parkinson’s disease (PD). Duplication and triplication of <i>SNCA</i> has been observed in PD patients, together with mutations at the N-terminal of the protein, among which A30P and A53T influence the formation of fibrils. By overexpressing human α-synuclein in the neuronal system of <i>Drosophila</i>, we functionally validated the ability of <i>IP3K2</i>, an ortholog of the GWAS identified risk gene, Inositol-trisphosphate 3-kinase B (<i>ITPKB</i>), to modulate α-synuclein toxicity in vivo. <i>ITPKB</i> mRNA and protein levels were also increased in SK-N-SH cells overexpressing wild-type α-synuclein, A53T or A30P mutants. Kinase overexpression was detected in the cytoplasmatic and in the nuclear compartments in all α-synuclein cell types. By quantifying mRNAs in the cortex of PD patients, we observed higher levels of <i>ITPKB</i> mRNA when <i>SNCA</i> was expressed more (<i>p</i> < 0.05), compared to controls. A positive correlation was also observed between <i>SNCA</i> and <i>ITPKB</i> expression in the cortex of patients, which was not seen in the controls. We replicated this observation in a public dataset. Our data, generated in SK-N-SH cells and in cortex from PD patients, show that the expression of α-synuclein and ITPKB is correlated in pathological situations.