Gan Shuoqiu, Sun Yingxiang, Liu Kejia, Jia Xiaoyan, Li Xuan, Zhang Ming, Bai Lijun
The Key Laboratory of Biomedical Information Engineering, Ministry of Education, Department of Biomedical Engineering, School of Life Science and Technology Xi'an Jiaotong University Xi'an China.
Institute of Artificial Intelligence Hefei Comprehensive National Science Center Hefei China.
Alzheimers Dement (Amst). 2024 Feb 16;16(1):e12550. doi: 10.1002/dad2.12550. eCollection 2024 Jan-Mar.
We evaluated how the apolipoprotein E () ε4 allele modulated the spatial patterns of longitudinal atrophy in the Alzheimer's disease-vulnerable brain areas of patients with mild traumatic brain injury (mTBI) from the acute to chronic phase post injury.
Fifty-nine adult patients with acute mTBI and 48 healthy controls with ε4 allele testing underwent T1-weighted magnetic resonance imaging and neuropsychological assessments with 6 to 12 months of follow-up. Progressive brain volume loss was compared voxel-wise in the temporal lobes.
Patients with the ε4 allele presented significant longitudinal atrophy in the left superior and middle temporal gyri, where the progressive gray matter volume loss predicted longitudinal impairment in language fluency, whereas mTBI ε4 allele noncarriers showed mainly significant longitudinal atrophy in the medial temporal lobes, without significant neuropsychological relevance.
The atrophy progression observed in mTBI patients with the ε4 allele may increase the possibility of developing a specific phenotype of Alzheimer's disease with language dysfunction.
The apolipoprotein E () ε4 allele and mild traumatic brain injury (mTBI) are risk factors for Alzheimer's disease (AD) progression.It is unclear how the interaction of mTBI with the ε4 allele impacts the progressive atrophy topography in AD-vulnerable brain regions.In this study, patients with the ε4 allele showed progressive atrophy patterns similar to the early stage of logopenic variant of primary progressive aphasia (lvPPA) phenotype of AD. ε4 allele carriers with mTBI history may be at the risk of developing a given AD phenotype with language dysfunction.
我们评估了载脂蛋白E(ApoE)ε4等位基因如何调节轻度创伤性脑损伤(mTBI)患者从损伤急性期到慢性期,在阿尔茨海默病易损脑区的纵向萎缩空间模式。
59名成年急性mTBI患者和48名进行了ε4等位基因检测的健康对照者接受了T1加权磁共振成像和神经心理学评估,并进行了6至12个月的随访。在颞叶以体素为单位比较渐进性脑容量损失。
携带ε4等位基因的患者在左侧颞上回和颞中回出现显著的纵向萎缩,其中渐进性灰质体积损失预示着语言流畅性的纵向损害,而mTBI非ε4等位基因携带者主要在内侧颞叶出现显著的纵向萎缩,与神经心理学无显著相关性。
在携带ε4等位基因的mTBI患者中观察到的萎缩进展可能增加发展为伴有语言功能障碍的阿尔茨海默病特定表型的可能性。
载脂蛋白E(ApoE)ε4等位基因和轻度创伤性脑损伤(mTBI)是阿尔茨海默病(AD)进展的危险因素。目前尚不清楚mTBI与ε4等位基因的相互作用如何影响AD易损脑区的渐进性萎缩地形。在本研究中,携带ε4等位基因的患者表现出与AD原发性进行性失语(lvPPA)表型的语言减少型变体早期阶段相似的渐进性萎缩模式。有mTBI病史的ε4等位基因携带者可能有发展为伴有语言功能障碍的特定AD表型的风险。