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Tau Hyperphosphorylation Assay
Neurofibrillary tangles (NFT) are aggregates of the microtubule-associated protein tau which has been hyperphosphorylated and accumulates inside the neuron. Tau proteins are the major components of intraneuronal and glial fibrillar lesions in numbers of neurodegenerative disorders referred to as ‘tauopathies’, including AD, frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Tau can undergo abnormal phosphorylation, truncation, or other modifications that result in the protein detachment from microtubules. These modified Tau molecules can self-associate and form different types of aggregates including neurofibrillary tangles (NFTs) found in brains of patients with neurodegenerative diseases such as Alzheimer’s disease. And the AD brain usually has a greater number of tau aggregates in specific cortical regions in particularly in the temporal lobe. Therefore, the development of novel compounds or antibodies that attenuate Tau hyperphosphorylation is an inevitable urgent.
Figure 1 A) Western blot tau phosphorylation assay: tau phosphorylation at two epitopes of Ser262 and Ser202/Thr205 (AT8) were analysed following 2 min ischaemia, 2 min ischaemia followed by 60 min recovery as well as 4 weeks recovery (n = 6 each). Total tau and actin levels are also examined. I-2m: 2 min ischaemia, I-2m/R- 60 m: 2 min ischaemia followed by 60 min reperfusion, I-2m/R- 4w: 2 min ischaemia followed by 4 weeks recovery period (One Way ANOVA, *p < 0.01, for p-tau (Ser262) in I-2m, I-2m/R- 60 m and I-2m/R- 4w vs control). Error bars depict the SD. All values are expressed as percent change relative to control group and were corrected by the Actin level. B) The presence of p-tau (Ser262), visualized by immunofluorescent staining which is mainly located in the processes in control group (a, b, c) and in soma and some parts of processes in the long-term recovery group of 2 min ischaemia followed by 4 weeks (d, e, f). DAPI (blue) shows nuclei staining. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Creative Bioarray offers diverse customized in vitro models to help our customers screen compounds that can preventing tau hyperphosphorylation. These in vitro models, including primary neuronal cultures and cell lines, are phenotypically closer to those observed in the aged neuronal network and mimic the development of AD.
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Reference
- Majd S.; et al. The impact of tau hyperphosphorylation at Ser 262 on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest. IBRO Reports. 2017, 2: 1-13.
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