SERUM ANTIBRAIN ENDOTHELIUM ANTIBODIES AND COGNITIVE ASSESSMENT IN PATIENTS WITH BINSWANGERS ENCEPHALOPATHY

The pathogenic mechanism underlying the vascular changes in Binswanger 's encephalopathy (BE) is unknown. To test whether alterations of the humoral immunity may lead to endothelium damage, we analyzed serum lev els of anti-brain endothelium antibodies (ABEA) (IgG and IgM) in 16 BE patients, 19 subjects with ischemic vascular diseases without mental deterioration and 18 normal healthy subjects. ABEA IgM were found elev ated in 1/16 (6%) BE patients and in 4/19 (21%) patients with cerebrov ascular diseases; an increase in ABEA IgM was found in 6/16 (38%) BE p atients and in 7/19 (37%) cerebrovascular patients. Association with a nti-cardiolipin antibodies (IgG and/or IgM) was found in 50% of BE pat ients with elevated ABEA and only 10% of those with no increase, where as high titres of anti-neurofilament antibodies (1:10 000) were detect ed in 40% and 71% respectively. In BE, ABEA IgG but not IgM showed a t rend, although not significant, towards a correlation with the duratio n of the disease (r(s) = 0.47; p = 0.07) and significantly correlated with the cognitive function as assessed by the Mini mental state (MMS) score (r(s) = 0.56; p = 0.02). Higher mean values of the MMS score we re found in BE patients with elevated ABEA than in those without (p = 0.04). This difference was not due to language disorders neither to an association with stroke risk factors or anti-neurofilament antibodies . However, there were no significant differences in MMS scores between cerebrovascular patients with ABEA and those without. A ''neuro-prote ctive'' role is hypothesized for the ABEA in the development of dement ia in BE.