RT期刊文章SR电子T1 CSF P-Tau181和其他生物标记神经元在细胞核内的夹杂物疾病患者摩根富林明神经病学神经学乔FD Lippincott Williams &威尔金斯SP e1009 OP e1019 10.1212 / WNL。首页100签证官0000000000201647是10 A1栗原市,Masanori A1小松,Hiroki A1仙谷由人,Renpei A1城市涩川市举行的Mari A1森本晃司,Satoru A1松原科技界A1荒川,彰A1 Orita, Makoto A1 Ishibashi吴克群A1 Mitsutake, Akihiko A1柴田则Shota A1 Ishiura, Hiroyuki A1足立,薰A1 Ohse, Kensuke A1波多野,Keiko A1 Ihara,恭子A1 Higashihara,法力A1仁科,靖A1 Tokumaru,阿雅美岛绿A1 Ishii,吴克群A1齐藤,裕A1 Murayama,茂雄A1 Kanemaru, Kazutomi A1岩田聪,Atsushi年2023 UL //www.ez-admanager.com/content/100/10/e1009.abstract AB背景和目标CSFτ181苏氨酸磷酸化(p-tau181)是一种广泛使用的生物标志物对阿尔茨海默病(AD)和最近被认为反映β-amyloid和/或p-tau沉积在大脑的广告。首页神经元在细胞核内的包含疾病(相当于卫生部)是一种神经退行性疾病,其特征是在核内包涵体神经元,神经胶质细胞和其他体细胞。症状包括老年痴呆症、神经病变等。脑脊液生物标志物没有报道。本研究的目的是调查是否改变了患者的CSF生物标志物包括p-tau181相当于卫生部。这是一个回顾性观察研究的方法。脑脊液浓度p-tau181,总τ,淀粉样β蛋白1-42 (Aβ42),单胺代谢产物高香草酸(HVA)和5-hydroxyindole乙酸(5-HIAA)之间的比较12日本国家传染病研究所患者120名老年痴呆症患者的临床综合征生物学证实基于脑脊液生物标志物概要文件,以及与其他神经认知障碍患者临床诊断(路易体痴呆与(下文),24;额颞叶痴呆FTD, 13;进行性核上的麻痹(PSP), 21个;和corticobasal综合症(CBS), 13)。 Amyloid PET using Pittsburgh compound B (PiB) was performed in 6 patients with NIID.Results The mean age of patients with NIID, AD, DLB, FTD, PSP, and CBS was 71.3, 74.6, 76.8, 70.2, 75.5, and 71.9 years, respectively. CSF p-tau181 was significantly higher in NIID (72.7 ± 24.8 pg/mL) compared with DLB, PSP, and CBS and was comparable between NIID and AD. CSF p-tau181 was above the cutoff value (50.0 pg/mL) in 11 of 12 patients with NIID (91.7%). Within these patients, only 2 patients showed decreased CSF Aβ42, and these patients showed negative or mild local accumulation in PiB PET, respectively. PiB PET scans were negative in the remaining 4 patients tested. The proportion of patients with increased CSF p-tau181 and normal Aβ42 (A−T+) was significantly higher in NIID (75%) compared with DLB, PSP, and CBS (4.2%, 4.8%, and 7.7%, respectively). CSF HVA and 5-HIAA concentrations were significantly higher in patients with NIID compared with disease controls.Discussion CSF p-tau181 was increased in patients with NIID without amyloid accumulation. Although the deposition of p-tau has not been reported in NIID brains, the molecular mechanism of tau phosphorylation or secretion of p-tau may be altered in NIID.5-HIAA=5-hydroxyindole acetic acid; AD=Alzheimer disease; Aβ42=amyloid-beta 1–42; ANCOVA=analysis of covariance; CBS=corticobasal syndrome; CL=centiloid; DLB=dementia with Lewy bodies; FAB=Frontal Assessment Battery; FXTAS=fragile X-associated tremor/ataxia syndrome; FTD=frontotemporal dementia; HSV-1=herpes simplex virus type 1; HVA=homovanillic acid; MAO=monoaminoxidase; MMSE=Mini-Mental State Examination; NIID=neuronal intranuclear inclusion disease; p-tau181=tau phosphorylated at threonine 181; PiB=Pittsburgh compound B; PSP=progressive supranuclear palsy; t-tau=total tau

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