The viruses used in this article from BrainVTA are in the table below

Intraneuronal accumulation of hyperphosphorylated tau is a hallmark pathology shown in over twenty neurodegenerative disorders, collectively termed as tauopathies, including the most common Alzheimer’s disease (AD). Therefore, selectively removing or reducing hyperphosphorylated tau is promising for therapies of AD and other tauopathies. Here, we designed and synthesized a novel DEPhosphorylation TArgeting Chimera (DEPTAC) to specifically facilitate the binding of tau to Bα-subunit-containing protein phosphatase 2A (PP2A-Bα), the most active tau phosphatase in the brain. The DEPTAC exhibited high efficiency in dephosphorylating tau at multiple AD-associated sites and preventing tau accumulation both in vitro and in vivo. Further studies revealed that DEPTAC significantly improved microtubule assembly, neurite plasticity, and hippocampus-dependent learning and memory in transgenic mice with inducible overexpression of truncated and neurotoxic human tau N368. Our data provide a strategy for selective removal of the hyperphosphorylated tau, which sheds new light for the targeted therapy of AD and related-tauopathies.

Figure 1. Sparse labeling of dentate granular cells by a mixture of AAVs.

In this study, the authors designed and synthesized here a novel DEPho-sphorylation targeting Chimaera (termed as DEPTAC) to selectively facilitate the link between tau and PP2A-Bα. By using the DEPTAC, a specific and efficient clearance of the AD-like hyperphosphorylated tau has been achieved both in vitro and in vivo. Which sheds new light for the targeted therapy of AD and related-tauopathies.
 
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