@article {Cicognola10.1212 / WNL。0000000000207358,作者={克劳迪娅Cicognola Niklas Mattsson-Carlgren和丹尼尔·西数和Henrik Zetterberg Kaj Blennow和塞巴斯蒂安Palmqvist Khazar艾哈迈迪Olof Strandberg和埃里克Stomrud Shorena Janelidze和奥斯卡·汉森},title ={协会的CSF PDGFRβ老化,血脑屏障损伤,神经炎症,和阿尔茨海默病病理变化},elocation-id = {10.1212 / WNL。={2023}0000000000207358},年,doi = {10.1212 / WNL。出版商0000000000207358}= {Wolters Kluwer健康,公司代表美国神经病学学会},文摘={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(C首页SF)。然而,目前尚不清楚如何周皮细胞损伤导致{\ textquoteright}年代老年痴呆症(广告)-相关变化和血脑屏障(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)和50.1 \ %是男性(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 = 2.8 - -3.9, p \ < 0.001)和GFAP (b = 27.4,β= 0.4,95 \ % CI = 20.9 - -33.9, p \ < 0.001),更糟的是BBB完整性衡量QAlb (b = 37.4,β= 0.2,95 \ % CI = 24.9 - -49.9, p < 0.001)。 Age was also associated with worse BBB integrity, and this was partly mediated by PDGFRβ and neuroinflammatory markers (16-33\% of total effect). 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.}, issn = {0028-3878}, URL = {//www.ez-admanager.com/content/early/2023/05/03/WNL.0000000000207358}, eprint = {//www.ez-admanager.com/content/early/2023/05/03/WNL.0000000000207358.full.pdf}, journal = {Neurology} }