■载脂蛋白和接触蛋白5是与阿尔茨海默病(AD)病理生理学相关的蛋白质。载脂蛋白在突触周转和终末增殖过程中作用于胆固醇和磷脂的转运和清除。接触蛋白5是参与神经发育关键过程的神经元膜蛋白。
■为了研究AD中contactin5与载脂蛋白之间的相互作用,以及这些蛋白质对神经元损伤的反应。
■载脂蛋白(通过Luminex测量),contactin5(通过Olink邻近延伸测定法测量),对认知未受损参与者(n=93)的脑脊液(CSF)和血浆中的胆固醇(通过液相色谱质谱法测定)进行了评估.使用聚合酶链反应在尸检确认的AD(n=57)和对照受试者(n=31)的额叶皮质中以及在内嗅皮层病变后的小鼠海马中测量基因表达。
■接触素5与载脂蛋白B呈正相关(p=5.4×10-8),D(p=1.86×10-4),E(p=2.92×10-9),J(p=2.65×10-9),和胆固醇(p=0.0096)在脑脊液中,和胆固醇(p=0.02),HDL(p=0.0143),和血浆中的LDL(p=0.0121)。在对照受试者的大脑中,CNTN5,APOB(p=0.034)和APOE(p=0.015)mRNA水平之间呈负相关。在老鼠模型中,apoe和apoj基因表达在神经支配期增加(p<0.05),而apob(p=0.023)和apod(p=0.006)在脱咖啡因阶段增加。
■在接触蛋白5和载脂蛋白和胆固醇之间观察到广泛的相互作用,可能是神经元损伤造成的.载脂蛋白基因表达的改变表明在轴突,终端,和响应内嗅皮层损伤的突触重塑。
UNASSIGNED: Apolipoproteins and contactin 5 are proteins associated with Alzheimer\'s disease (AD) pathophysiology. Apolipoproteins act on transport and clearance of cholesterol and phospholipids during synaptic turnover and terminal proliferation. Contactin 5 is a neuronal membrane protein involved in key processes of neurodevelopment.
UNASSIGNED: To investigate the interactions between contactin 5 and apolipoproteins in AD, and the role of these proteins in response to neuronal damage.
UNASSIGNED: Apolipoproteins (measured by Luminex), contactin 5 (measured by Olink\'s proximity extension assay), and cholesterol (measured by liquid chromatography mass spectrometry) were assessed in the cerebrospinal fluid (CSF) and plasma of cognitively unimpaired participants (n = 93). Gene expression was measured using polymerase chain reaction in the frontal cortex of autopsied-confirmed AD (n = 57) and control subjects (n = 31) and in the hippocampi of mice following entorhinal cortex lesions.
UNASSIGNED: Contactin 5 positively correlated with apolipoproteins B (p = 5.4×10-8), D (p = 1.86×10-4), E (p = 2.92×10-9), J (p = 2.65×10-9), and with cholesterol (p = 0.0096) in the CSF, and with cholesterol (p = 0.02), HDL (p = 0.0143), and LDL (p = 0.0121) in the plasma. Negative correlations were seen between CNTN5, APOB (p = 0.034) and APOE (p = 0.015) mRNA levels in the brains of control subjects. In the mouse model, apoe and apoj gene expression increased during the reinnervation phase (p < 0.05), while apob (p = 0.023) and apod (p = 0.006) increased in the deafferentation stage.
UNASSIGNED: Extensive interactions were observed between contactin 5 and apolipoproteins and cholesterol, possibly due to neuronal damage. The alterations in gene expression of apolipoproteins suggest a role in axonal, terminal, and synaptic remodeling in response to entorhinal cortex damage.