A translational study showed that the Parkinson’s-linked LRRK2 R1627P mutation amplifies gut inflammation and promotes α‑synuclein aggregation in rat models. Investigators reported increases in intestinal immune activation and pathological α‑synuclein—features implicated in early Parkinson’s disease progression. The result bolsters the gut–brain hypothesis of Parkinson’s and underscores LRRK2 as a multi‑compartment target; drugs that modulate LRRK2 kinase activity could have implications for both central and peripheral disease processes. The data may inform biomarker strategies and patient selection for LRRK2-directed clinical trials.