Elecsys® Phospho-Tau (181P) CSF

ElectroChemiLuminescence Immunoassay (ECLIA) for the in vitro quantitative determination of phosphorylated Tau in human Cerebrospinal Fluid (CSF)

Tau (tubulin-associated unit) protein is one of the two hallmarks of Alzheimer’s disease, besides β-Amyloid (1-42) (Abeta42). During neurodegeneration abnormal phosphorylation leads to formation of intracellular neurofibrillary tangles (NFTs) composed of the Tau protein that has undergone hyper-phosphorylation, and developed aggregates of hyper-phosphorylated Tau proteins called Phospho-Tau (pTau)^1,2

The Elecsys Phospho-Tau (181P) CSF assay is designed to detect the protein or fragments of Tau protein phosphorylated at threonine 181 in human CSF.

Many studies show that high CSF pTau levels is associated with a faster progression from Mild Cognitive Impairment (MCI) to AD with more rapid cognitive decline in AD patients³ and in mild AD dementia cases.⁴ CSF pTau levels increase around 2 – 3 fold in mild‑moderate AD patients compared to age‑matched controls, while CSF β‑Amyloid (1‑42) (Abeta42) levels decrease to around half the level in controls.^5,6

Elecsys^®Phospho-Tau (181P) CSF (pTau) is an in vitro diagnostic immunoassay intended for the quantitative determination of the phosphorylated tau protein concentration in human cerebrospinal fluid (CSF).⁷

Elecsys^® pTau assay is part of the Elecsys^® AD portfolio, along with Elecsys^® β-Amyloid(1-42) CSF II (AB42 2) and Elecsys^® Total-Tau CSF (tTau) immunoassays.⁷

Elecsys^® AD CSF assays can detect amyloid positivity, enhancing diagnostic accuracy and physician confidence.^8,9

Elecsys^® AD CSF assays enable timely intervention by identifying patients with MCI at risk of progression to AD.^7,9

References

Iqbal, K., Liu, F., Gong, CX. (2016). Nat Rev Neurol, 12(1), 15-27.
Wang, Y., Mandelkow, E. (2016). Nat Rev Neurosci, 17(1), 5-21.
Blom, ES., Giedraitis, V., Zetterberg, H. et al. (2009). Dement Geriatr Cogn Disord, 27(5), 458-64.
Snider, BJ., Fagan, AM., Roe, C. et al. (2009). Arch Neurol, 66(5), 638-45.
Mattsson, N., Zetterberg, H., Hansson, O., et.al. (2009). JAMA 22, 302(4), 385-93.
Hampel, H., Blennow, K. (2004). Dialogues Clin Neurosci,6(4), 379-390.
Elecsys® Method Sheet: ms_08821941500V1.0, ms_08821909500V1.0, ms_08846715500V1.0, ms_08846693500V1.0, ms_08846634500V1.0, ms_08846685500V1.0
Rabinovici, G.D. et al. (2019). Association of Amyloid Positron Emission Tomography With Subsequent Change in Clinical Management Among Medicare Beneficiaries With Mild Cognitive Impairment or Dementia. JAMA 321(13), 1286-1294.
Hansson, O. et al. (2018). CSF biomarkers of Alzheimer’s disease concord with amyloid-β PET and predict clinical progression: A study of fully automated immunoassays in BioFINDER and ADNI cohorts. Alzheimers Dement 14(11), 1470-1481