CSF phosphorylated tau as an indicator of subsequent tau accumulation

Petrice M. Cogswell, Heather J. Wiste, Michelle M. Mielke, Christopher G. Schwarz, Stephen D. Weigand, Val J. Lowe, Terry M. Therneau, David S. Knopman, Jonathan Graff-Radford, Prashanthi Vemuri, Matthew L. Senjem, Jeffrey L. Gunter, Alicia Algeciras-Schimnich, Ronald C. Petersen, Clifford R. Jack

Research output: Contribution to journalArticlepeer-review


We evaluated the relationship between baseline CSF p-tau181 and the rate of tau PET change in the temporal meta-ROI and entorhinal cortex (ERC) and how it varied by amyloid level (CSF Aβ42 or amyloid PET) among 143 individuals from the Mayo Clinic Study of Aging and Mayo Alzheimer Disease Research Center. Higher CSF p-tau181, lower CSF Aβ42, and higher amyloid PET levels were associated with faster rates of tau PET change in both the temporal meta-ROI and ERC. In the temporal meta-ROI, longitudinal tau PET accumulation occurred primarily in participants with abnormal biomarker levels and a diagnosis of dementia, which supports the hypothesis that tau aggregation begins later in the disease process. Compared to the temporal meta-ROI, the ERC showed greater change in tau PET in non-demented participants but less change in later disease stages, supporting ERC as a more sensitive marker of early tau PET changes but with less dynamic range over the disease spectrum. We found both amyloid and CSF p-tau181 were associated with rates of tau PET change but there were some differences in associations by region, amyloid biomarker, and disease stage.

Original languageEnglish (US)
Pages (from-to)189-200
Number of pages12
JournalNeurobiology of aging
StatePublished - Sep 2022


  • Alzheimer Disease
  • CSF p-tau
  • amyloid
  • tau PET

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology


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