T-lymphocyte tumor necrosis factor-alpha receptor binding in patients with Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disease of the central nervous system (CNS), in which the cytokine network may be deranged, leading to an altered immunoregulation. Tumor necrosis factor(TNF)-alpha, a cytokine with pleiotropic neuroimmune effects, has specific receptors on human lymphocytes, as well as on other cell types, even in the CNS. The aim of the present study was to assay TNF-alpha binding on peripheral blood T cells from PD patients, as compared with healthy subjects. We found on T lymphocytes from parkinsonian patients significantly more TNF-alpha receptors than on those from controls (B (max): 637+/-23 vs. 131+/-6 (mean+/-S.E.M.) receptors/cell). Such TNF-alpha binding sites are of the same type in patients and healthy subjects (K(d): 66.8+/-5.1 vs. 70.7+/-5.6 (mean+/-S.E.M.) pM). These results are discussed in terms of PD immunopathogenesis, since it has been reported that activated T lymphocytes have increased amounts of TNF-alpha receptors.

Human blood platelet as research tool in neuropsychopharmacology.

The use of blood platelets as a nerve terminal model for serotonin is well documented. However, it is clear that the use of platelets as a model can be justified only for those parameters where it may be shown that blood platelets and neural cells share almost identical features. The excellent similarity between the serotonin transport mechanisms in platelets and in nerve terminals, and the existence of various receptors for biogenic amines, peptides and substances with neuronal activity on platelet membrane offer a really unique opportunity to utilize blood platelets as a system for drug evaluation. In our work platelet benzodiazepine binding sites and their modulation by different benzodiazepines in normals and in demented patients are examined.