p-Tau 217

How it works?

Alzheimer’s disease (AD) is a neurodegenerative disorder hallmarked by extracellular amyloid-beta (AB) plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau (p-tau), which lead to progressive loss of neuronal function and cell death (1). These pathologies can be present and developing in the brain for years before any symptoms become apparent (2). During this buildup there are several specific proteins that are released into the cerebrospinal fluid (CSF) that have been identified as reliable biomarkers for the diagnosis of AD.

Tau protein normally acts to stabilize the axons of neurons, but when it is hyperphosphorylated (p-tau) it becomes prone to aggregating into neurofibrillary tangles, leading to neuronal dysfunction and death (3), There are several variants of p-tau that have been identified as significant in AD, differentiated by the location of the phosphorylation site.

The two most notable isoforms are p-tau 181 and p-tau 217. Levels of p-tau 181 and 217 in both CSF and blood have been shown to be elevated in AD and increase over the course of the disease, indicating they could be a valuable tool for diagnosis (4,5), but the relative performance of the two has been an area of intense interest.

Studies have consistently found that p-tau 217 levels are more sensitive and specific than p-tau 181 levels in distinguishing between AD and other neurodegenerative disorders (5-7). p-tau-217 also shows greater correlation with tau- and amyloid-positron emission tomography (PET) imaging, gold standards for detecting AD pathology in the brain (6,7).

Our assay is a single analyte, ultra-sensitive Simoa immunoassay for the accurate quantification of p-tau 217 levels in blood. This cutting-edge technique analyzes plasma samples with an automated system of sample preparation, data collection, and analysis. Results are reported in pg/mL and include an interpretation based on normal p-tau 217 concentration ranges.


  • 1. Ittner LM, Götz J. Amyloid-β and tau—a toxic pas de deux in Alzheimer’s disease. Nature Reviews Neuroscience. 2011 Feb;12(2):67-72.

  • 2. Thal DR et al. Pathology of clinical and preclinical Alzheimer’s disease. European archives of psychiatry and clinical neuroscience. 2013 Nov;263:137-45.

  • 3. Iqbal K et al. Tau pathology in Alzheimer disease and other tauopathies. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease. 2005 Jan 3;1739(2-3):198-210.

  • 4. Brickman AM et al. Correlation of plasma and neuroimaging biomarkers in Alzheimer’s disease. Annals of clinical and translational neurology. 2022 May;9(5):756-61.

  • 5. Thijssen EH et al. Association of Plasma P-tau217 and P-tau181 with clinical phenotype, neuropathology, and imaging markers in Alzheimer’s disease and frontotemporal lobar degeneration: a retrospective diagnostic performance study. The Lancet. Neurology. 2021 Sep;20(9):739.

  • 6. Yu L et al. Plasma p-tau181 and p-tau217 in discriminating PART, AD and other key neuropathologies in older adults. Acta Neuropathologica. 2023 Apr 9:1-1.

  • 7. Leuzy A et al. Comparing the clinical utility and diagnostic performance of CSF P-Tau181, P-Tau217, and P-Tau231 assays. Neurology. 2021 Oct 26;97(17):e1681-94.