Department of Gerontology and Metabolism, Charles University in Prague, Medical Faculty and University Hospital, Hradec Kralové, Czech Republic.
J Nutr Health Aging. 2010 Nov;14(9):758-61. doi: 10.1007/s12603-010-0325-1.
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.
免疫系统和内皮细胞的衰老可能导致与年龄相关的血管和神经退行性疾病，包括阿尔茨海默病。本研究的目的是评估转化生长因子β（TGFβ）和可溶性内皮糖蛋白（sCD105）的血清水平与神经退行性变之间的潜在关系，以及这些分子在衰老过程中的变化。
研究对象包括三组，第一组是 63 名健康的中年参与者，31 名女性，32 名男性，平均年龄 35 岁。第二组由 58 名健康、独立生活在养老院的居民组成，44 名女性，14 名男性，平均年龄 83.5 岁。第三组包括 129 名阿尔茨海默病患者，86 名女性，43 名男性，平均年龄 80 岁，MMSE 评分为 16-20。
采用 ELISA 法，用商业试剂盒检测外周血中 TGFβ和可溶性内皮糖蛋白的含量。
健康年轻组血清 TGFβ水平为 34339±6420pg/ml，健康老年组为 37555±11944pg/ml，阿尔茨海默病患者为 29057±11455pg/ml。与健康老年人相比，阿尔茨海默病患者的 TGFβ血清水平显著降低（p<0.01）。健康年轻组血清内糖蛋白水平为 4.88±0.95μg/ml，健康老年组为 6.11±1.38μg/ml，阿尔茨海默病患者为 7.20±1.72μg/ml。与年轻对照组相比，老年健康人血清内糖蛋白水平显著升高（p<0.001）。与健康老年人相比，阿尔茨海默病患者的血清内糖蛋白水平显著升高（p<0.001）。
阿尔茨海默病患者 TGFβ水平降低可能导致脑循环受损，表现为内糖蛋白水平升高。这些发现可能表明免疫系统参与了阿尔茨海默病的发病机制。
