Neurofibrillary tangles (NFTs) are one of the key pathological hallmarks of Alzheimer’s disease. NFTs primarily consist of phosphorylated tau (pTau). In the healthy brain tau binds to microtubules, providing stability and facilitating axonal transport (Mandelkow and Mandelkow, 2012; Sotiropoulos et al., 2017).

Dec 3, 2024 · Plasma p-tau217 has proven to be an excellent biomarker for AD pathology due to its close association with both brain Aβ and tau pathology, as well as its large dynamic range.

Plasma pTau181 identified amyloid β-PET positive individuals regardless of clinical diagnosis and correlated with cortical tau protein deposition measured by 18 F-Flortaucipir PET. Plasma pTau181 may be useful to screen for tau pathology associated with AD.

DNA is shown in blue using the DAPI stain which highlights the nuclei. Image courtesy EnCor Biotechnology Inc. Tau proteins are found more often in neurons than in non-neuronal cells in humans.

AD2 anti-pTau labels the so-called astrocytic tufts, corresponding to intra-cytoplasmic Tau aggregation in astrocytes (arrow, left panel). Tau E2 and Tau E10 show glial Tau pathology as well, astrocytic (upper right, arrow) or oligodendrial (arrowhead, lower right).

Detecting pTau in the blood is now being used as a way to diagnose Alzheimer's disease earlier and more accurately. This research breakthrough is critical because the earlier Alzheimer’s disease is detected, the more potential options for intervention are available.

Jun 7, 2019 · Alzheimer’s disease neuropathologic change (ADNC) is defined by progressive accumulation of β-amyloid plaques and hyperphosphorylated tau (pTau) neurofibrillary tangles across diverse regions of brain.

Oct 17, 2017 · Here we found that in human samples obtained post TBI due to a variety of causes, cis P-tau is induced in cortical axons and cerebrospinal fluid and positively correlates with axonal injury and...

Jan 9, 2025 · Here we present on the development, validation, and clinical utility of Janssen’s plasma p217+tau Simoa assay. The assay was initially created for CSF in 2017 and used as a pharmacodynamic marker in the Ph1 posdinemab trials, demonstrating substantial dose dependent reduction in CSF p217+tau.

Here, we hypothesized that neurons that degenerate in the earliest stages of sAD (1) strongly express ApoER2 and (2) show evidence of ApoER2-Dab1 disruption through co-accumulation of multiple RAAAD-P-LTP components.