Tau (tubulin-associated unit) protein is one of the two hallmarks of Alzheimer’s disease (AD), 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 are 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
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