午睡
氯氮平
精神分裂症(面向对象编程)
基因剔除小鼠
神经保护
抗精神病药
药理学
内科学
医学
内分泌学
神经科学
生物
精神科
受体
作者
Avia Merenlender‐Wagner,Regina Pikman,Eliezer Giladi,Annie Andrieux,Illana Gozes
出处
期刊:Peptides
[Elsevier]
日期:2010-07-01
卷期号:31 (7): 1368-1373
被引量:53
标识
DOI:10.1016/j.peptides.2010.04.011
摘要
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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