Year: 2025
Type: article
Abstract: BACKGROUND: Tau PET enables longitudinal tracking of the trajectory of AD tauopathy with respect both to signal intensity and anatomic location. Typically beginning in a specific, small area of the medial temporal lobe (MTL), the rhinal cortex, deposition of tau fibrils increases with increasing amyloid-β (Aβ) burden at first slowly then catastrophically to neocortex in association with cognitive decline. However, both the anatomy and PET signal intensity are heterogeneous across individuals, with some showing, e.g., a more rapid rise in tau deposition at lower levels of amyloidosis. METHOD: We have been able to characterize such heterogeneity in two longitudinal studies of pre-clinical AD, the Harvard Aging Brain Study (HABS; mean(sd) follow-up duration 3.3(2.3)yr) and the A4 study (3.3(1.8)y). RESULT: Among those with Aβ >24CL (N = 229), those who also had tau > 1.2 SUVr (N = 112, 49%) had increasing tau; below this tau threshold, spread of tau PET signal to neocortical regions was not detected during the follow-up interval (slope ∼0). CONCLUSION: These analyses may be useful for clinical trial enrollment targeting specific phases of the AD tau progression trajectory.
Source: Alzheimer s & Dementia
Author: Keith A. Johnson
Institutions: Harvard University, Massachusetts General Hospital
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,200
OpenAlex ID: W7117251144
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