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surfen and oxalyl surfen decrease tau hyperphosphorylation and mitigate neuron deficits in vivo in a zebrafish model of tauopathy

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Translational Neurodegeneration 2018年第1期7卷 54-62页

作者： Seyedeh Maryam Alavi Naini Constantin Yanicostas Rahma Hassan-Abdi Sébastien Blondeel Mohamed Bennis Ryan J.Weiss Yitzhak Tor Jeffrey D.Esko Nadia Soussi-Yanicostas PROTECT InsermUniversitéParis DiderotSorbonne Paris CitéParisFrance Institut de Biologie Paris Seine-Laboratoire Neuroscience Paris Seine Inserm UMRS 1130CNRS UMR 8246UPMC UM 118UniversitéPierre et Marie CurieParisFrance Cadi Ayyad University MarrakeshMorocco Department of Chemistry and Biochemistry University of CaliforniaSan DiegoLa JollaCAUSA Department of Cellular and Molecular Medicine University of CaliforniaSan DiegoLa JollaCAUSA

Background:Tauopathies comprise a family of neurodegenerative disorders including Alzheimer’s disease for which there is an urgent and unmet need for disease-modifying *** are characterized by pathological tau hyperphosphorylation,which has been shown to correlate tightly with disease progression and memory loss in patients suffering from Alzheimer’s *** recently demonstrated an essential requirement for 3-O-sulfated heparan sulfate in pathological tau hyperphosphorylation in zebrafish,a prominent model organism for human drug ***,we investigated whether in vivo treatment with surfen or its derivatives oxalyl surfen and hemisurfen,small molecules with heparan sulfate antagonist properties,could mitigate tau hyperphosphorylation and neuronal deficits in a zebrafish model of ***:In vivo treatment of Tg[HuC::hTau^(P301L);DsRed]embryos for 2 days with surfen or oxalyl surfen significantly reduced the accumulation of the pThr181 tau phospho-epitope measured by ELISA by 30%and 51%,*** blot analysis also showed a significant decrease of pThr181 and pSer396/pSer404 in embryos treated with surfen or oxalyl *** analysis further confirmed that treatment with surfen or oxalyl surfen significantly decreased the AT8 tau epitope in spinal *** addition,in vivo treatment of Tg[HuC::hTau^(P301L);DsRed]embryos with surfen or oxalyl surfen significantly rescued spinal motoneuron axon-branching defects and,as a likely consequence,the impaired stereotypical touch-evoked escape ***,treatment with hemisurfen,a surfen derivative devoid of heparan sulfate antagonist activity,does not affect tau hyperphosphorylation,nor neuronal or behavioural deficits in Tg[HuC::hTau^(P301L);DsRed]***:Our findings demonstrate for the first time that surfen,a well-tolerated molecule in clinical settings,and its derivative,oxalyl surfen,could mitigate or delay neuronal defects

关键词： Tauopathy Zebrafish Alzheimer’s disease Tau protein Tau hyperphosphorylation surfen Oxalyl surfen Heparan sulfate

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