Monogenic mouse models of autism spectrum disorders: Common mechanisms and missing links.
Monogenic mouse models of autism spectrum disorders: Common mechanisms and missing links.
复制标题
DOI：
10.1016/j.neuroscience.2015.12.040
复制
发表时间：
2016-05-03
期刊：
影响因子：
3.3
通讯作者：
Jiang YH
中科院分区：
文献类型：
--
作者：
Hulbert SW;Jiang YH
自闭症谱系障碍（ASD）在遗传学和神经生物学领域提出了独特的挑战，因为这些疾病的临床和分子异质性。在ASD患者中发现的基因突变提供了使用动物模型剖析自闭症行为背后的分子和电路机制的机会。正在进行的转基因模型的研究提供了关键的洞察可能的共同机制所产生的不同的突变，但分子异常和行为表型之间的联系仍然难以捉摸。在小鼠自闭症建模中遇到的挑战需要一种新的分析范式，该范式将行为分析与电路水平分析整合在具有较强结构效度的转基因模型中。
Autism Spectrum Disorders (ASDs) present unique challenges in the fields of genetics and neurobiology because of the clinical and molecular heterogeneity underlying these disorders. Genetic mutations found in ASD patients provide opportunities to dissect the molecular and circuit mechanisms underlying autistic behaviors using animal models. Ongoing studies of genetically modified models have offered critical insight into possible common mechanisms arising from different mutations, but links between molecular abnormalities and behavioral phenotypes remain elusive. The challenges encountered in modeling autism in mice demand a new analytic paradigm that integrates behavioral analysis with circuit-level analysis in genetically modified models with strong construct validity.