Strittmatter M, Hamann G F, Grauer M T, Cramer H, Schimrigk K
Department of Neurology, University of Saarland, Homburg, Germany.
Dement Geriatr Cogn Disord. 1997 Jan-Feb;8(1):34-42. doi: 10.1159/000106598.
In 21 patients suffering from Binswanger's disease (BD) and in 53 patients suffering from Alzheimer's disease, we measured cerebrospinal fluid (CSF) concentrations of somatostatin-like immunoreactivity (SLI), high molecular weight form somatostatin (HMV-SST), somatostatin-25/28 (SST-25/28), somatostatin-14 (SST-14), Des-ala-somatostatin (Des-ala-SST), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). The patients were classified into three stages of intellectual deterioration according to the global deterioration scale (GDS). Levels of SLI were significantly decreased in BD in general and in SDAT patients with severe dementia (GDS 7), compared to a control group (BD overall 19.7 +/- 11.6 fmol/ml, SDAT 18.6 +/- 7.9 vs. 30.5 +/- 8.6 fmol/ml in controls, p < 0.01 for both). In SDAT patients, SLI levels correlated with dementia scores (r = -0.65, p < 0.05), but not in BD. HVA levels were decreased significantly in SDAT and BD patients with severe dementia (SDAT 273.5 +/- 138.7, BD 224.3 +/- 69.9 vs. 364.9 +/- 103.8 nmol/ml, p < 0.01 in controls, p < 0.05 for both). In BD patients with light dementia (GDS 2-4), HVA levels were significantly elevated (p < 0.05). In BD, HVA levels correlated with dementia (r = -0.59, p < 0.01). 5-HIAA was significantly elevated in BD patients with light dementia (p < 0.05). Qualitative and quantitative changes in the molecular forms of SLI are compatible with a dysregulated posttranslational processing SDAT and BD. We also observed significant correlations between SLI, 5-HIAA and HVA in BD indicating a neurochemical heterogeneous and generalized process affecting several transmitter systems and functions. In summary, our study shows that despite their quite different neuropathology, SDAT and BD do not differ fundamentally in their neurochemical profile.
在21例患有宾斯旺格病（BD）的患者和53例患有阿尔茨海默病的患者中，我们测量了脑脊液（CSF）中生长抑素样免疫反应性（SLI）、高分子量形式生长抑素（HMV-SST）、生长抑素-25/28（SST-25/28）、生长抑素-14（SST-14）、去丙氨酸生长抑素（Des-ala-SST）、高香草酸（HVA）和5-羟吲哚乙酸（5-HIAA）的浓度。根据总体衰退量表（GDS）将患者分为智力衰退的三个阶段。与对照组相比，BD患者总体以及重度痴呆（GDS 7）的阿尔茨海默病（SDAT）患者的SLI水平显著降低（BD总体为19.7±11.6 fmol/ml，SDAT为18.6±7.9 vs.对照组的30.5±8.6 fmol/ml，两者均p<0.01）。在SDAT患者中，SLI水平与痴呆评分相关（r = -0.65，p<0.05），但在BD患者中不相关。重度痴呆的SDAT和BD患者的HVA水平显著降低（SDAT为273.5±138.7，BD为224.3±69.9 vs.对照组的364.9±103.8 nmol/ml，对照组p<0.01，两者均p<0.05）。轻度痴呆（GDS 2-4）的BD患者中，HVA水平显著升高（p<0.05）。在BD中，HVA水平与痴呆相关（r = -0.59，p<0.01）。轻度痴呆的BD患者中5-HIAA显著升高（p<0.05）。SLI分子形式的定性和定量变化与SDAT和BD中翻译后加工失调相一致。我们还观察到BD中SLI、5-HIAA和HVA之间存在显著相关性，表明这是一个影响多个递质系统和功能的神经化学异质性和全身性过程。总之，我们的研究表明，尽管SDAT和BD的神经病理学有很大不同，但它们的神经化学特征并无根本差异。
