Purpose: Hereditary parkinsonism genes consist of causative genes of familial Parkinson’s disease (PD) with a locus symbol prefix (PARK genes) and hereditary atypical parkinsonian disorders that present atypical features and limited responsiveness to levodopa (non-PARK genes). Although studies have shown that hereditary parkinsonism genes are related to idiopathic PD at the phenotypic, gene expression, and genomic levels, no study has systematically investigated connectivity among the proteins encoded by these genes at the protein-protein interaction (PPI) level. Materials and Methods: Topological measurements and physical interaction enrichment were performed to assess PPI networks constructed using some or all the proteins encoded by hereditary parkinsonism genes (n=96), which were curated using the Online Mendelian Inheritance in Man database and literature. Results: Non-PARK and PARK genes were involved in common functional modules related to autophagy, mitochondrial or lysosomal organization, catecholamine metabolic process, chemical synapse transmission, response to oxidative stress, neuronal apoptosis, regulation of cellular protein catabolic process, and vesicle-mediated transport in synapse. The hereditary parkinsonism proteins formed a single large network comprising 51 nodes, 83 edges, and three PPI pairs. The probability of degree distribution followed a power-law scaling behavior, with a degree exponent of 1.24 and a correlation coefficient of 0.92. LRRK2 was identified as a hub gene with the highest degree of betweenness centrality; its physical interaction enrichment score was 1.28, which was highly significant. Conclusion Both PARK and non-PARK genes show high connectivity at the PPI and biological functional levels.

Colonic duplication constitutes a rare congenital anomaly, characterized by the presence of hollow cystic or tubular structures exhibiting an epithelial-lined intestinal wall. Diagnostic challenges persist due to its low incidence and manifestation of nonspecific symptoms such as abdominal pain or constipation, resulting in a reluctance to pursue surgical resection. As associated malignancies in colonic duplication are rare, the inherent malignant potential of these anomalies remains undetermined. Additionally, despite reported instances of associated malignancies in colonic duplication, there is an absence of reports in the literature detailing tubular adenoma within these cases. The histologic features of the presented case are particularly noteworthy, situated at the precancerous stage, intimating potential progression towards adenocarcinoma within colonic duplication.