Neurochemical differences in the CSF between Binswanger's andAlzheimer's disease
M. Strittmatter
Bok Engelsk 1997
| Utgitt | 1997
|
|---|---|
| Omfang | Side 34- 42
|
| Opplysninger | In 21 patients suffering from Binswanger's disease (ED) and in 53patients suffering from Alzheimer's disease, we measuredcerebrospinal fluid (CSF) concentrations of somatostatin-likeimmunoreactivity (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 intothree stages of intellectual deterioration according to the globaldeterioration scale (GDS). Levels of SLI were significantly decreasedin ED in general and in SDAT patients with severe dementia (GDS 7),compared to a control group (BD overall 19.7 +/- 11.6 fmol/ml, SDAT18.6 +/- 7.9 vs. 30.5 +/- 8.6 fmol/ml in controls, p < 0.01 forboth). In SDAT patients, SLI levels correlated with dementia scores(r = -0.65, p < 0.05), but not in ED. HVA levels were decreasedsignificantly in SDAT and ED patients with severe dementia (SDAT273.5 +/- 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 ED patients with lightdementia (GDS 2-4), HVA levels were significantly elevated (p <0.05). In ED, HVA levels correlated with dementia (r = -0.59, p <0.01). 5-HIAA was significantly elevated in ED patients with lightdementia (p < 0.05). Qualitative and quantitative changes in themolecular forms of SLI are compatible with a dysregulatedposttranslational processing in SDAT and ED. We also observedsignificant correlations between SLI, 5-HIAA and HVA in ED indicatinga neurochemical heterogeneous and generalized process affectingseveral transmitter systems and functions. In summary, our studyshows that despite their quite different neuropathology, SDAT and EDdo not differ fundamentally in their neurochemical profile.
|
| Emner |
