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NAP (davunetide) enhances cognitive behavior in the STOP heterozygous mouse--a microtubule-deficient model of schizophrenia.

Abstract : NAP (generic name, davunetide) is an active fragment of activity-dependent neuroprotective protein (ADNP). ADNP-/- embryos exhibit CNS dysgenesis and die in utero. ADNP+/- mice survive but demonstrate cognitive dysfunction coupled with microtubule pathology. NAP treatment ameliorates, in part, ADNP-associated dysfunctions. The microtubule, stable tubule-only polypeptide (STOP) knockout mice were shown to provide a reliable model for schizophrenia. Here, STOP-/- as well as STOP+/- showed schizophrenia-like symptoms (hyperactivity) that were ameliorated by chronic treatment with the antipsychotic drug, clozapine. Daily intranasal NAP treatment significantly decreased hyperactivity in the STOP+/- mice and protected visual memory.
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https://www.hal.inserm.fr/inserm-00498115
Contributor : Annie Andrieux <>
Submitted on : Thursday, April 28, 2011 - 5:57:40 PM
Last modification on : Thursday, March 26, 2020 - 6:57:37 PM
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Avia Merenlender-Wagner, Regina Pikman, Eliezer Giladi, Annie Andrieux, Illana Gozes. NAP (davunetide) enhances cognitive behavior in the STOP heterozygous mouse--a microtubule-deficient model of schizophrenia.. Peptides, Elsevier, 2010, 31 (7), pp.1368-73. ⟨10.1016/j.peptides.2010.04.011⟩. ⟨inserm-00498115⟩

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