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Mass spectrometry measures of plasma Aβ, tau and P‐tau isoforms’ relationship to amyloid PET, tau PET, and clinical stage of Alzheimer’s disease

Recent advances in understanding the links between amyloid‐beta (Aβ) and specific tau isoforms in brain, cerebrospinal fluid (CSF), and blood indicate that a cascade of events of Alzheimer’s disease (AD) pathophysiology begin with detection of altered CSF and blood Aβ 42/40 ratio, followed by increases in amyloid plaques by Positron Emission Tomography (PET) scan, associated with increased phosphorylation of specific CSF tau isoforms (e.g. p‐tau217 and p‐tau181), before increases in p‐tau205, hypometabolism, and atrophy. Finally, CSF total tau increases before tau aggregation by tau PET and onset of clinical symptoms. The longitudinal tau and Aβ changes which occur in brain and CSF are now being understood in blood, enabling interpretation and understanding of AD progression in much larger and more robust populations.