Heat‑shock proteins deter Alzheimer’s tau

A man with a deterministic Alzheimer’s mutation shows heavy amyloid but almost no tau and no cognitive decline. He has unusually high heat‑shock proteins—possibly from years working in 110°F Navy engine rooms—along with low inflammation and distinct gene variants. This suggests boosting chaperone responses could block tau pathology even when amyloid is present. — If inducible heat‑shock pathways can interrupt the amyloid→tau cascade, Alzheimer’s prevention might include chaperone‑enhancing drugs or controlled stressors, reframing therapeutic targets and occupational/exposure research.