The bivariate distribution of amyloid-β and tau: relationship with established neurocognitive clinical syndromes

Author:

Jack Clifford R1ORCID,Wiste Heather J2,Botha Hugo3ORCID,Weigand Stephen D2,Therneau Terry M2,Knopman David S3,Graff-Radford Jonathan3,Jones David T13,Ferman Tanis J4,Boeve Bradley F3ORCID,Kantarci Kejal1,Lowe Val J5,Vemuri Prashanthi1,Mielke Michelle M6,Fields Julie A7,Machulda Mary M7,Schwarz Christopher G1,Senjem Matthew L1,Gunter Jeffrey L1,Petersen Ronald C3

Affiliation:

1. Department of Radiology, Mayo Clinic, Rochester, MN, USA

2. Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA

3. Department of Neurology, Mayo Clinic, Rochester, MN, USA

4. Department of Psychology, Mayo Clinic, Jacksonville, FL, USA

5. Department of Nuclear Medicine, Mayo Clinic, Rochester, MN, USA

6. Department of Epidemiology, Mayo Clinic, Rochester, MN, USA

7. Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA

Abstract

See Gordon and Tijms (doi:10.1093/brain/awz278) for a scientific commentary on this article. Jack et al. examine relationships between the bivariate distribution of β-amyloid and tau on PET and established neurocognitive clinical syndromes. Amyloidosis appears to be required for high levels of 3R/4R tau deposition. Whereas abnormal amyloid PET is compatible with normal cognition, highly abnormal tau PET is not.

Funder

National Institutes of Health

GHR Foundation

Publisher

Oxford University Press (OUP)

Subject

Neurology (clinical)

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