RT期刊文章SR电子T1协会的CSF PDGFRβ老化,血脑屏障损伤,神经炎症,阿尔茨海默病病理变化摩根富林明神经病学神经学乔FD Lippincott Williams &威尔金斯10.1212 SP / WNL。首页0000000000207358 10.1212 / WNL。0000000000207358 A1克劳迪娅Cicognola A1 Niklas Mattsson-Carlgren A1丹尼尔·西数A1 Henrik Zetterberg A1 Kaj Blennow A1塞巴斯蒂安Palmqvist A1 Khazar艾哈迈迪A1 Olof Strandberg A1 Erik Stomrud A1 Shorena Janelidze A1奥斯卡·汉森年2023 UL //www.ez-admanager.com/content/early/2023/05/03/WN首页L.0000000000207358.abstract AB背景和目标受伤的周神经血管单元释放血小板源生长因子β(PDGFRβ)脑脊液(CSF)。然而,目前尚不清楚如何周皮细胞损伤导致阿尔茨海默病(AD)有关的变化和血脑屏障(BBB)的伤害。我们旨在测试如果CSF PDGFRβ与不同的广告,与年龄有关的病理变化导致痴呆。方法测量771年CSF PDGFRβ认知正常(铜、n = 408),轻度认知障碍(MCI, n = 175)和痴呆科目(n = 188)的瑞典BioFINDER-2队列。然后我们检查协会Aβ-PET和tau-PET SUVR, APOEε4基因型和核磁共振测量皮质厚度、白质病变(WML)和脑血流量(CBF)。我们也分析了角色的CSF PDGFRβ老化之间的关系,BBB功能障碍(CSF /血浆白蛋白比率衡量QAlb)和神经炎症(即。、YKL-40 CSF水平和神经胶质原纤维酸性蛋白(GFAP),优先在反应性星形胶质细胞表达)。结果队列的平均年龄67年(铜= 62.8、MCI = 69.9、痴呆= 70.4),50.1%为男性(铜= 46.6%,MCI = 53.7%,痴呆= 54.3%)。CSF PDGFRβ浓度是高年龄(b = 19.1,β= 0.5,95% CI = 16 - 22.2, p < 0.001),增加脑脊液神经炎症标志物胶质激活YKL-40 (b = 3.4,β= 0.5,95% CI -3.9 = 2.8, p < 0.001)和GFAP (b = 27.4,β= 0.4,95% CI -33.9 = 20.9, p < 0.001),更糟的是BBB完整性衡量QAlb (b = 37.4,β= 0.2,95% CI -49.9 = 24.9, p < 0.001)。年龄也是BBB完整性较差,这部分是由PDGFRβ和神经炎症标记(16 - 33%的总效应)。 However, PDGFRβ showed no associations with APOE ε4 genotype, PET imaging of Aβ and tau pathology or MRI measures of brain atrophy and white matter lesions (p>0.05).Discussion In summary, pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathological changes.

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