A newly reported LRRK2 R1627P mutation markedly amplifies gut inflammation and α‑synuclein aggregation in rat models, implicating a genetically driven gut pathology in early Parkinson’s disease processes. Complementing that work, teams published a 3D gut‑brain‑vascular platform in Nature Communications that models bidirectional signaling between the gut, vasculature and brain, offering a translational tool to probe mechanisms like those driven by LRRK2 variants. The pair of studies link a defined genetic lesion to gut‑driven neuropathology and provide an experimental system to test causality and interventions. α‑Synuclein aggregation is a core Parkinson’s pathology; these findings prioritize gut inflammation and barrier biology as targets for early‑stage disease modification research.