At follow-up, cognition in PD remained lower than in controls by 1.1–1.3 MoCA points—statistically robust but modest in magnitude—while biomarker profiles differed consistently between groups and evolved over time (higher p-tau and Aβ42 in controls; a narrowing and slight reversal in p-tau/Aβ42 by V08). The gene discussed is MAPT; the disease is Parkinson disease.