Dementia of Alzheimer type (DAT) is a neurodegenerative disease of the
central nervous system (CNS), in which an unbalanced cytokine network
may lead to an altered immunoregulation. Tumour necrosis factor (TNF)
-alpha is a cytokine with manifold effects on the neuroimmune system.
Specific TNF-alpha receptors have been found on human peripheral blood
lymphocytes. The aim of the present study has been to assay TNF-alpha
binding on T cells from DAT patients and healthy sex- and age-matched
controls. We found that T lymphocytes from demented patients bear sig
nificantly more p60 and p80 TNF-alpha receptors than those from contro
ls (B-max: 705, 29 vs 131, 6 (mean, SEM) receptors/cell). Such TNF-alp
ha binding sites, of the same type in BAT patients and healthy subject
s (Kd: 67.6, 5.0 vs 70.7, 5.6 (mean, SEM) pM, are functional, since th
ey are able to mediate in vitro NF-kappa B activation. These results a
re discussed in terms of DAT pathogenesis. Since it has been reported
that activated T cells have more TNF-alpha receptors than resting cell
s, an increased number of lymphocyte TNF-alpha receptors might indicat
e a systemic immune activation in DAT patients as compared with health
y controls.