Akkaoui Juliet, Devadoss Dinesh, Wang Hongjie, Movila Alexandru, Lakshmana Madepalli K
Department of Cellular and Molecular Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, Florida, USA.
Department of Chemistry and Biochemistry, Center for Molecular Biology and Biotechnology, Institute for Human Health and Disease Intervention (I-HEALTH), Florida Atlantic University, Jupiter, Florida, USA.
J Cell Mol Med. 2025 Jul;29(13):e70686. doi: 10.1111/jcmm.70686.
Emerging studies indicate that the IQ-motif-containing protein K (IQCK) is a novel risk factor for Alzheimer's disease (AD), an age-associated disease. The expression patterns of IQCK in healthy and AD brains, within the context of age and sex are largely unknown. Therefore, we compared the age-dependent expression patterns of IQCK in males and females of wild-type (WT) mice with AD-like 3xTg and APΔE9 mice. Additionally, we measured IQCK protein expression in AD-derived human iPSC neurons. In WT mice, we found no IQCK expression at day 1 (1D) in the cortex (CX), hippocampus (HP), brainstem (BS) and cerebellum (CB). Overall, IQCK protein expression in different brain regions was first detected in 1-month-old wild-type (WT) mice, reaching its maximum in 1-year-old mice (1Y), and then gradually decreased in 2-year-old mice. In the APΔE9 mice, IQCK protein levels significantly increased by 1246% in the CX, 682% in the HP and 169% in the BS relative to WT controls. In the 3xTg mice, only HP showed an increase of IQCK protein by 277%. In addition, we also detected elevated tendencies in BS and CB regions but not in the CX. Finally, IQCK expression was also significantly increased by 68% in the AD-derived iPSC neurons relative to the NC-derived iPSC neurons. Thus, increased IQCK protein levels in the brain of AD-like 3xTg and APΔE9 mouse models suggest a possible role in AD pathogenesis, a finding that requires further clarification.
新兴研究表明,含IQ模体蛋白K(IQCK)是阿尔茨海默病(AD)这一与年龄相关疾病的新型风险因素。在年龄和性别的背景下,IQCK在健康大脑和AD大脑中的表达模式在很大程度上尚不清楚。因此,我们比较了野生型(WT)小鼠、AD样3xTg小鼠和APΔE9小鼠的雄性和雌性中IQCK的年龄依赖性表达模式。此外,我们测量了源自AD的人诱导多能干细胞(iPSC)神经元中IQCK蛋白的表达。在WT小鼠中,我们在第1天(1D)时未在皮质(CX)、海马体(HP)、脑干(BS)和小脑(CB)中检测到IQCK表达。总体而言,不同脑区的IQCK蛋白表达首先在1月龄野生型(WT)小鼠中被检测到,在1岁小鼠(1Y)中达到最大值,然后在2岁小鼠中逐渐下降。在APΔE9小鼠中,相对于WT对照组,CX中的IQCK蛋白水平显著增加了1246%,HP中增加了682%,BS中增加了169%。在3xTg小鼠中,只有HP显示IQCK蛋白增加了277%。此外,我们还在BS和CB区域检测到升高趋势,但在CX中未检测到。最后,相对于源自正常对照(NC)的iPSC神经元,源自AD的iPSC神经元中IQCK表达也显著增加了68%。因此,AD样3xTg和APΔE9小鼠模型大脑中IQCK蛋白水平的升高表明其在AD发病机制中可能起作用,这一发现需要进一步阐明。