Anschuetz Anne, Schwab Karima, Harrington Charles R, Wischik Claude M, Riedel Gernot
School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
TauRx Therapeutics Ltd, Aberdeen, UK.
J Alzheimers Dis. 2025 Aug 1;107(2):13872877251362212. doi: 10.1177/13872877251362212.
BackgroundSynaptic proteins are often used as markers for synaptic damage in non-clinical models of Alzheimer's disease (AD) and are known to be affected early in the disease in humans. Presynaptic protein loss has been shown to be especially strong in patients, though not all proteins and brain areas are affected equally.ObjectiveTo investigate whether presynaptic protein loss is similarly heterogenous in non-clinical AD models, a meta-analysis was conducted in rodent models of the disease.MethodsPubMed, Embase, and Medline databases were searched for publications measuring presynaptic markers in AD rodent model brains between 2015-2023. A total of 1333 records arose from the searches, and these were screened for suitable studies. Meta-analyses on global presynaptic protein changes, protein-, area- and model-specific effects amongst others were performed on 184 studies. Studies employing proteomic approaches for protein quantification were analyzed separately from non-proteomic studies.ResultsRobust and significant global loss of presynaptic proteins was observed in these animal models. The effect size varied between different model types, with the greatest effects being observed in models in which either tau was genetically modified or where amyloid-β injection was used. The greatest severity was seen in hippocampal subregions and for proteins associated with the vesicle release machinery (SNARE proteins).ConclusionsProteomic studies confirmed that presynaptic proteins were most frequently lower in AD models relative to control, although some proteins were increased. Multiple presynaptic proteins were found to be altered in proteomic meta-analysis and some of these may constitute putative biomarkers that warrant further investigation.
背景
突触蛋白常被用作阿尔茨海默病(AD)非临床模型中突触损伤的标志物,且已知在人类疾病早期会受到影响。尽管并非所有蛋白质和脑区受到的影响都相同,但已表明突触前蛋白的丢失在患者中尤为明显。
目的
为了研究在非临床AD模型中突触前蛋白的丢失是否同样具有异质性,对该疾病的啮齿动物模型进行了一项荟萃分析。
方法
在PubMed、Embase和Medline数据库中搜索2015年至2023年间测量AD啮齿动物模型大脑中突触前标志物的出版物。搜索共产生1333条记录,并对这些记录进行筛选以找出合适的研究。对184项研究进行了关于整体突触前蛋白变化、蛋白质、区域和模型特异性效应等方面的荟萃分析。采用蛋白质组学方法进行蛋白质定量的研究与非蛋白质组学研究分开分析。
结果
在这些动物模型中观察到突触前蛋白出现了显著且明显的整体丢失。不同模型类型之间的效应大小有所不同,在tau基因被修饰或使用淀粉样β注射的模型中观察到的效应最大。在海马亚区域以及与囊泡释放机制相关的蛋白质(SNARE蛋白)中观察到的严重程度最高。
结论
蛋白质组学研究证实,与对照组相比,AD模型中突触前蛋白最常降低,尽管有些蛋白质有所增加。在蛋白质组学荟萃分析中发现多种突触前蛋白发生了改变,其中一些可能构成值得进一步研究的假定生物标志物。