Analysis of 1,356 participants from the 1946 British birth cohort found essentially no associations between antibodies against 14 common pathogens and plasma p-tau217 levels or brain amyloid-beta accumulation measured seven years later. The study examined lifetime exposure markers for infections including herpes viruses, cytomegalovirus, and Helicobacter pylori in people aged 60-64, then tracked Alzheimer's disease biomarkers at age 70. Only herpes simplex virus 2 showed any relationship—unexpectedly linked to lower tau levels—while modest interactions emerged between certain pathogens and APOE ε4 genetic risk. These null findings challenge the popular "antimicrobial protection hypothesis," which suggests brain amyloid plaques form defensively against infections, subsequently triggering tau pathology. The research contradicts several smaller studies linking infections to dementia risk, though observational cohort studies cannot definitively establish causation. As a preprint awaiting peer review, these results require validation, but they represent some of the strongest evidence against infection-driven Alzheimer's pathology in a well-characterized population. The findings suggest infectious disease prevention may have limited impact on core Alzheimer's brain changes, though broader cognitive health benefits remain possible.