脉冲前抑制
神经认知
睡眠剥夺
精神分裂症(面向对象编程)
睡眠剥夺对认知功能的影响
抗精神病药
精神病
药物开发
认知
生物标志物
拟精神病
神经科学
医学
药品
睡眠(系统调用)
心理学
精神科
内科学
生物
生物化学
NMDA受体
受体
计算机科学
操作系统
作者
Ulrich Ettinger,Veena Kumari
标识
DOI:10.1016/s2215-0366(15)00313-2
摘要
Development of drugs for the treatment of the clinical symptoms and cognitive deficits of schizophrenia is unsatisfactory, with many initially promising compounds not showing beneficial effects in clinical studies. Experimental model systems of schizophrenia combined with well-validated biomarkers are urgently needed to provide early indicators of effectiveness. Herein, we argue that experimentally controlled sleep deprivation represents a translational model system that can be studied in combination with neurocognitive biomarkers. Specifically, we review data on the psychotomimetic effects of sleep deprivation in healthy human beings and provide evidence of the psychosis-like deficits in translational inhibitory biomarkers-prepulse inhibition and antisaccades-that occur after sleep deprivation. These data support the use of the sleep deprivation model in combination with biomarkers with excellent psychometric properties and well-characterised neural mechanisms, such as prepulse inhibition and antisaccades, to substantially advance development of drugs with antipsychotic or pro-cognitive effects.
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