Department of Neurology, Medisch Centrum Leeuwarden, The Netherlands.
Departments of Clinical Chemistry, Amsterdam University Medical Center location VUmc, Alzheimer Center, Amsterdam, The Netherlands.
J Alzheimers Dis. 2019;71(1):15-20. doi: 10.3233/JAD-190344.
To investigate amyloid-β (Aβ) in frontotemporal dementia (FTD), cerebrospinal fluid (CSF) Aβ38, Aβ40, and Aβ42 in frontotemporal lobar degeneration (FTLD; N = 18 genetically and/or pathologically confirmed and N = 8 FTD with concomitant amyotrophic lateral sclerosis) were compared with Alzheimer's disease (AD; pathological or Pittsburgh-compound-B Positron-emission-tomography (PIB-PET) positive; N = 25) and controls (N = 24). For all the Aβ subtypes, group difference was seen and post-hoc analysis revealed lower levels in FTLD compared to controls (p≤0.05). Aβ42/40 ratio showed no difference between FTLD and controls; however, a difference was seen between AD versus FTLD (p < 0.01). This is an intriguing finding, suggesting a possible role of Aβ in FTLD pathogenesis.
为了研究额颞叶痴呆（FTD）中的淀粉样蛋白-β（Aβ），我们比较了额颞叶变性（FTLD；N=18 例经基因和/或病理证实和 N=8 例伴有肌萎缩侧索硬化的 FTD）与阿尔茨海默病（AD；病理或匹兹堡复合物-B 正电子发射断层扫描（PIB-PET）阳性；N=25）和对照组（N=24）的脑脊液（CSF）Aβ38、Aβ40 和 Aβ42。所有 Aβ亚型均存在组间差异，事后分析显示 FTLD 组的水平低于对照组（p≤0.05）。FTLD 与对照组之间 Aβ42/40 比值无差异，但 AD 与 FTLD 之间存在差异（p<0.01）。这是一个有趣的发现，提示 Aβ 在 FTLD 发病机制中可能起作用。
