Association of Amyloid and Tau With Cognition in Preclinical Alzheimer Disease

By Bernard J. Hanseeuw, Rebecca A. Betensky, H. Jacobs, A. Schultz, Jorge Sepulcre, J. Becker, Danielle M. Cosio, Michelle E. Farrell, Y. Quiroz, E. Mormino and 12 more. JAMA Neurology, 2019

751 citations recorded by the source corpus.

Key Points Question Is cognitive decline associated with amyloid-β or tau tangles accumulation? Findings In this cohort study that included 60 normal older adults with repeated positron emission tomography measures, the rate of tau accumulation in the inferior temporal neocortex was associated with the rate of cognitive decline. Amyloid accumulation was associated with subsequent tau accumulation, and this sequence of successive amyloid and tau changes in neocortex was found to mediate the association of initial amyloid with final cognition, measured 7 years later. Meaning Amyloid positron emission tomography is useful to detect early Alzheimer pathology; repeated tau positron emission tomography is useful to track disease progression.

Subfields: Physiology, Psychiatry and Mental health, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/f255b534cc740d86a1b2bd64395815df9e1a1c34

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In Physiology

1. J. Long
2. D. Holtzman
3. Berislav Zlokovic

In Psychiatry and Mental health

1. J. Long
2. D. Holtzman

Citations in the corpus

• Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, positive): “accumulation of tau was a predictor of cognitive impairment, whereas the presence or accumulation of amyloid was a predictor of more severe tau-associated cognitive impairment (Aschenbrenner et al., 2018; Hanseeuw et al., 2019).”
• Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future (2023, background): “As the upstream factor, Aβ triggered the hyperphosphorylation of tau protiens, which synergistically induced neuronal impairment and cognitive deficits.(111,115) Aβ accelerated the tau hyperphosphorylation by the activation of cyclindependent kinase 5 (CDK5) and glycogen synthase kinase 3 (GSK-3).”