CSF somatostatin increase in patients with early parkinsonian syndrome

Abstract

Somatostatin-like immunoreactivity levels (SLI) in cerebrospinal fluid (CSF) were determined in twenty-three patients with untreated parkinsonian syndrome (15 with Idiopathic Parkinson's disease (IPD) and 8 with other forms of parkinsonism) at the moment of clinical diagnosis (mean duration of disease 1.1 +/- 0.2 years), and in 26 subjects without neurological symptoms. None of the IPD patients had a diagnosis of dementia at the moment of inclusion in the study. CSF-SLI content was found to be significantly higher in patients with parkinsonian syndrome (107.9 +/- 9.8 pg/ml) than in control subjects (73.5 +/- 8.4 pg/ml). The increase was also significant when controls were compared with IPD patients. In addition, a positive correlation between SLI and homovanillic acid was found in CSF of all patients. A test of learning memory was used to evaluate the mental state of patients and a significant increase in CSF-somatostatin levels was observed in patients with Idiopathic Parkinson's disease and severe affectation of memory. These results indicate that in the early steps of untreated parkinsonian syndrome, somatostatin concentration in cerebrospinal fluid may increase, probably due to the neurodegenerative depletion of somatostatin from striatal or cortical neurons.

Diagnostic cerebrospinal fluid biomarkers for Parkinson's disease: A pathogenetically based approach

“…A potential explanation for this decrease is cell death of specific neurons or suppression of their secretory activity (Strittmatter et al, 1996). Cell death may on the other hand result in increased levels of neuropeptides through the release of peptides from damaged brain tissue (Espino et al, 1995). Raised CSF peptide levels have been demonstrated for diazepam binding inhibitor (DBI) (Ferrero et al, 1988a,b) and des-ala-somatostatin (Strittmatter et al, 1996).…”

“…Raised CSF peptide levels have been demonstrated for diazepam binding inhibitor (DBI) (Ferrero et al, 1988a,b) and des-ala-somatostatin (Strittmatter et al, 1996). Several neuropeptides have been reported only once and the results of some neuropeptide studies led to conflicting data (Dupont et al, 1982;Espino et al, 1995;Jolkkonen et al, 1986;Strittmatter et al, 1996;Strittmatter and Cramer, 1992;Unger et al, 1988).…”

Somatostatin prevents lipopolysaccharide-induced neurodegeneration in the rat substantia nigra by inhibiting the activation of microglia

“…In addition, the decreased SST levels in the frontal and entorhinal cortex as well as the hippocampus have been correlated to the cognitive deficits in patients with PD ( 9 ). However, increases in SST have been observed in the cerebrospinal fluid of patients with early PD ( 10 ). Due to the controversial data reported, the function and mechanism of SST which participates in PD are still subject to extensive examination.…”

Somatostatin and Cognitive Function in Neurodegenerative Disorders

“…SST mRNA quantitation revealed a significant increase in the medial medullary lamina of the globus pallidus in PD relative to the controls, suggesting a specific modification of basal ganglia SS-ergic pathways in PD [149,150]. However, conflicting evidence has also been published, the results pointing either to a SLI elevation in the CSF [151] or to no changes in SLI post mortem in the cerebral cortex [152,153] or in cortical neurosurgical biopsies [154], suggesting that involvement of the SST-ergic system may not be a primary and consistent neurochemical feature of dementia [155], or at least it may be less significant than in AD dementia [156]. Conversely, monitoring of the levels of SST in the serum or brain samples has been used in the animal models, or during the treatment of the disease [157,158].…”