Transforming growth factor beta and soluble endoglin in the healthy senior and in Alzheimer's disease patients.

Abstract

Senescence of the immune system and of endothelial cells can contribute to age-dependent vascular and neurodegenerative disorders including Alzheimer's disease. The aim of this study is an assessment of putative relationships of serum levels of transforming growth factor beta (TGFβ) and soluble endoglin (sCD105) and neurodegeneration, and of changes of these molecules in the course of ageing. The subjects of the study consisted of three groups, the first one was 63 otherwise healthy middle - aged participants, 31 females, 32 males, of average age 35 years. The second group was formed by 58 healthy, self-dependent inhabitants of nursing homes, 44 females and 14 males, average age 83.5 years. The third group comprised of 129 Alzheimer's disease patients, 86 females, 43 males, of average age 80 years, with MMSE score that ranged from 16 to 20. Serum levels of TGF beta and soluble endoglin were measured by the ELISA method in samples of peripheral blood using commercial kits. The serum level of TGFβ was 34,339 ± 6,420 pg/ml in the healthy younger group, 37,555 ± 11,944 pg/ml in the healthy seniors, and 29,057 ± 11,455 pg/ml in Alzheimer's disease patients. Compared to healthy seniors, the serum level of TGFβ was significantly decreased in Alzheimer's disease patients (p < 0.01). The serum level of endoglin were 4.88 ± 0.95 μg/ml in the healthy younger group; 6.11 ± 1.38 μg/ml in healthy seniors, and 7.20 ± 1.72 μg/ml in patients with Alzheimer's disease, respectively. The serum level of endoglin was significantly higher (p < 0.001) in senescent healthy persons compared to the younger control group. When compared with healthy seniors, patients with Alzheimer's disease had significantly elevated (p < 0.001) serum level of endoglin. Decreased levels of TGF β in Alzheimer's disease may result in impairment of cerebral circulation reflected in the increased endoglin levels. These findings may indicate involvement of the immune system in Alzheimer's disease pathogenesis.