Guo Daji, Yang Xiaoman, Gao Ming, Chen Xiaoqing, Tang Yanping, Shen Lingling, Li Keshen, Shi Lei
Clinical Neuroscience Institute, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
JNU-HKUST Joint Laboratory for Neuroscience and Innovative Drug Research, College of Pharmacy, Jinan University, Guangzhou, 510632, Guangdong, China.
Cell Mol Neurobiol. 2023 Apr;43(3):1129-1146. doi: 10.1007/s10571-022-01233-4. Epub 2022 May 30.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that lasts lifelong and causes noticeably higher premature mortality. Although the core symptoms and other behavioral deficits of ASD can persist or be deteriorated from early development to old age, how aging affects the behaviors and brain anatomy in ASD is largely unknown. DOCK4 is an ASD risk gene highly expressed in the hippocampus, and Dock4 knockout (KO) mice display ASD-like behaviors in adulthood (4- to 6-month-old). In this study, we evaluated the behavioral and hippocampal pathological changes of late-middle-aged (15- to 17-month-old) Dock4 male KO mice. Aged Dock4 KO mice continuously showed similar social deficit, elevated anxiety, and disrupted object location memory as observed in the adulthood, when compared to their wild-type (WT) littermates. Notably, Dock4 KO mice displayed an age-related decline of hippocampal dependent spatial memory, showing decreased spatial memory in Barnes maze than their WT littermates at late middle age. Morphological analysis from WT and Dock4 KO littermates revealed that Dock4 deficiency led to decreased mature neurons and oligodendrocytes but increased astrocytes in the hippocampus of late-middle-aged mice. Together, we report that ASD-like behaviors mostly persist into late-middle age in Dock4 KO mice, with specific alterations of spatial memory and hippocampal anatomy by age, thus providing new evidence for understanding age differences in behavioral deficits of ASD.
自闭症谱系障碍(ASD)是一种神经发育障碍,会持续终生,并导致明显更高的过早死亡率。尽管ASD的核心症状和其他行为缺陷从早期发育到老年都可能持续存在或恶化,但衰老如何影响ASD患者的行为和脑解剖结构在很大程度上尚不清楚。DOCK4是一种在海马体中高表达的ASD风险基因,Dock4基因敲除(KO)小鼠在成年期(4至6个月大)表现出类似ASD的行为。在本研究中,我们评估了中老年(15至17个月大)雄性Dock4基因敲除小鼠的行为和海马体病理变化。与野生型(WT)同窝小鼠相比,老年Dock4基因敲除小鼠持续表现出与成年期相似的社交缺陷、焦虑加剧和物体定位记忆障碍。值得注意的是,Dock4基因敲除小鼠表现出海马体依赖性空间记忆的年龄相关性下降,在中老年期的巴恩斯迷宫实验中,其空间记忆能力低于野生型同窝小鼠。对野生型和Dock4基因敲除同窝小鼠的形态学分析表明,Dock4基因缺失导致中老年小鼠海马体中成熟神经元和少突胶质细胞数量减少,但星形胶质细胞数量增加。总之,我们报告Dock4基因敲除小鼠中类似ASD的行为大多持续到中老年期,且空间记忆和海马体解剖结构随年龄出现特定变化,从而为理解ASD行为缺陷的年龄差异提供了新证据。