Together with convergent evidence from human neuronal cultures and AD+ mouse models, our findings position Chlamydia pneumoniae as an amplifier of AD pathology and dysfunction and highlight pathogen- and NLRP3-targeted strategies, including timely antibiotic and inflammasome-modulating interventions, as testable routes to modify disease progression and accelerate development of accessible retinal imaging biomarkers of infection-linked AD burden. The gene discussed is NLRP3; the disease is infection.