Frisoni and colleagues review experimental and clinical data that stress increases Alzheimer risk and accelerates the disease by directly promoting amyloid, tau, and neuroinflammation. Ironically, as core stress circuits degenerate, physiological stress markers grow less interpretable—unhinged from subjective experience. The pursuit of “stress biomarkers” for AD will remain a foggy business, useful in theory but resistant to easy operationalization.
Stress as Both Risk and Mechanism in Alzheimer’s Disease: The Unruly Biomarker
How do chronic stress and breakdowns in stress neuroendocrine systems muddy the waters of Alzheimer’s disease causation, progression, and biomarker interpretation?