Alzheimer's disease (AD) is characterized by extensive deposition of amyloid (A ) and formation of neurofibrillary tangles (NFTs) consisting of hyperphosphorylated Tau. So far, a variety of AD drugs targeting A have been developed, but ended in failure. A recent focus on AD therapy, therefore, is development of Tau-targeted drugs. A activates glycogen synthase kinase-3 (GSK-3 ), that plays a central role in Tau phosphorylation, responsible for NFT formation. The linoleic acid derivative DCP-LA

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... as been developed as a promising drug for AD therapy. DCP-LA serves as a selective activator of PKC and a potent inhibitor of protein tyrosine phosphatase 1B (PTP1B). DCP-LA restrains Tau phosphorylation efficiently due to PKC -mediated direct inactivation of GSK-3 , to PKC /Akt-mediated inactivation of GSK-3 , and to receptor tyrosine kinase/insulin receptor substrate 1/phosphoinositide 3-kinase/3phosphoinositide-dependent protein kinase 1/Akt-mediated inactivation of GSK-3 in association with PTP1B inhibition. Moreover, DCP-LA ameliorates spatial learning and memory impairment in 5xFAD transgenic mice, an animal model of AD. Consequently, combination of PKC activation and PTP1B inhibition must be an innovative strategy for AD therapy.