Somatostatin, its Molecular Forms and Monoaminergic Transmitter Metabolites in Binswanger's Disease. Neurochemical-Neuropathological Considerations

Abstract

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) were measured in 21 patients with Binswanger's dementia (BD). Patients were classed into three stages of intellectual deterioration according to the Global de-terioration scale (GDS). Levels of SLI were significantly decreased in patients suffering from BD, compared to a control group (19.7 ± 11.6 fmol/ml vs. 30.5 ± 8.6 fmol/ml,P< 0.01). There was no correlation with dementia scores (r= 0.34,P= 0.51). The observed qualitative and quantitative changes in the molecular pattern of SLI suggest the occurrence of a dysregulated posttranslational processing in patients with BD. Whereas 5-HIAA levels were not significantly changed in patients with BD, HVA was significantly increased in mild to moderate dementia (GDS 2-4) and significantly decreased in severe cases (GDS 7) (224.3 ± 69.9 nmol/ml vs. 364.9 ± 103.8 nmol/ml,P< 0.01); this correlated with dementia scores (r= −0.59,P< 0.01). The existence of significant correlations between SLI, 5-HIAA and HVA in BD point to a heterogeneous and generalized neurochemical process affecting several transmitter systems and functions.