A NON-HUMAN PRIMATE AUTISM MODEL BASED ON MATERNAL IMMUNE ACTIVATION

基于母体免疫激活的非人灵长类自闭症模型

• 批准号: 8172560
• 负责人: PAUL H PATTERSON
• 金额: $ 11.41万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8172560
• 关键词: Animals; Anxiety; Autistic Disorder; Behavioral; Cerebellum; Communication; Computer Retrieval of Information on Scientific Projects Database; Epidemiology; Exhibits; Facial Expression; Funding; Grant; Human; Impairment; Institution; Investigation; Modeling; Mus; Pregnant Women; Primates; Purkinje Cells; Research; Research Personnel; Resources; Respiratory Tract Infections; Risk; Series; Social Behavior; Social Interaction; Source; Therapeutic Intervention; United States National Institutes of Health; Virus Diseases; Work; base; immune activation; mouse model; neuropathology; nonhuman primate; novel; offspring; pregnant

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Based on epidemiological evidence that viral infection of pregnant women can strongly increase the risk for autism in their offspring, a mouse model of maternal immune activation has been established. Pregnant mice are given a respiratory infection at midgestation, and the offspring display a series of behavioral abnormalities consistent with those seen in autism, including deficits in social interaction and investigation of novel objects, as well as increased anxiety under mildly stressful conditions. Moreover, these offspring exhibit a specific type of neuropathology that is often seen in autism: spatially localized deficit of Purkinje cells in the cerebellum. Now that the mouse model has shown behavioral and histological abnormalities consistent with those found in autism, it is important to extend this work to primates. These animals possess a behavioral repertoire, such as the expression and interpretation of facial expressions, which is very homologous with human social behavior. Non-human primates therefore provide a sensitive indicator of impairments in social behavior and communication. A valid primate model of autism would also provide a unique resource for evaluating therapeutic interventions.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 基于流行病学证据，表明孕妇的病毒感染可以强烈增加其后代自闭症的风险，因此已经建立了母体免疫激活的小鼠模型。怀孕的小鼠在中间疗法时患有呼吸道感染，后代表现出与自闭症中看到的一系列行为异常，包括社交互动和对新物体的调查的缺陷以及在轻度压力条件下的焦虑增加。此外，这些后代表现出一种特定类型的神经病理学类型，通常在自闭症中可以看到：小脑中浦肯野细胞的空间局部缺陷。现在，小鼠模型已经显示出与自闭症中发现的行为和组织学异常相一致的，因此将这项工作扩展到灵长类动物很重要。这些动物具有行为曲目，例如面部表情的表达和解释，这与人类的社会行为非常同源。因此，非人类灵长类动物提供了社会行为和沟通障碍的敏感指标。自闭症的有效灵长类动物模型还将为评估治疗干预措施提供独特的资源。