Background. The occurrence of mixed dementia defined as the association of Alzheimer's disease with vascular dementia is increasing due to the global aging of the human population. Since thyroid hormones play a role in cognition and alterations of the thyroid axis occur with aging it is reasonable to assume that thyroid function and cognitive decline in mixed dementia are linked.Objective. To investigate whether there is a link between TSH, oxidative stress, cognitive decline and depression in female patients with mixed dementia.Methods. Fourty female patients with mixed dementia and 10 healthy controls were included in the study. MMSE, depression score (Cornel Scale of depression), TSH, MDA, glutathione were determined. Serum TSH levels correlated with the cognitive decline measured by MMSE (r=0.55 p=0.0002) and with de depression score (r=0.34 p=0.0314). Furthermore an increase in the oxidative stress marker MDA (p=0.0004) and in the antioxidant defense marker Glutathione (p=0.0013) was observed in patients with mixed dementia. In addition the levels of Glutathione correlated with cognitive decline (r=-0.4997 p=0.001) and with the levels of TSH (r=-0.4997 p=0.001).Conclusion. Our results suggest that thyroid function, oxidative stress and mixed dementia are corelated. However, a possible cause and effect relationship is not yet proved.

We have studied the short-term and long-term effects of a single dose of Dexamethasone upon the nervous system. Studies have been performed with 2 groups of 15 Wistar rats: I (control), 11-2i/g Dexamethasone i.p., during the first 24 hours of life. At 3 days old, we sacrificed 5 animals from each group; the others performed functional tests at 3 months old and then were sacrificed. At 3 days and 3 months old, we explored: the histological disorders, the neuronal viability, the cytochrome oxidase activity, the Mg-dependent ATPase activity from the cerebral cortex, hippocampus and hypothalamus, and oxidative stress parameters from the homogenates. Our results indicate the presence of immediate morphological, enzymatic and oxidative stress disorders in all the brain structures, partially reversible until the age of 3 months.

Environmental iodine deficiency continues to be a significant public health problem worldwide. On the other hand, iodide excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. For this reason we intended to explore iodide excess impairment on prooxidant/antioxidant balance of the thyroid gland, hepatic tissue and in blood and the effect of selenium administration on oxidative stress markers under the same circumstances. Experiments were performed for 10 days with white, male, Wistar rats, as follows: group 1: control-normal iodine supply group; 2: high iodine diet, group; 3: high iodine diet and selenium; group 4: high iodine diet and Carbimasole. Oxidative stress markers such as lipid peroxides were determined in thyroid gland, hepatic tissue and in blood. Measuring H+ donor ability of the sera and catalase activity in thyroid gland and in hepatic tissue assessed antioxidant defense. Iodide excess had prooxidant effects, leading to an increased lipid peroxides level and catalase activity in target tissues and in blood and to a decreased H+ donor ability of the sera. Selenium supplementation had opposite effects. Present data allow us to conclude that the alterations due to iodide excess in thyroid gland, hepatic tissue and in blood are mediated through oxidative stress.

The purpose of this study was to examine the dynamic of oxidative stress in patients with hyperthyroidism before and during treatment with carbimazole using the measurement of malondialdehyde as marker of oxidative stress and ceruloplasmine as antioxidant in blood serum. In eleven female patients with diagnosed Basedow disease and nine healthy controls subjects (eight females and one male) marker of oxidative stress (malondialdehyde) and antioxidant (ceruloplasmine) were estimated before and during the treatment with carbimazole. We observed increased concentration of these parameters in blood serum before the treatment and their normalization after the carbimazole treatment. These results suggest that this drug can be used as an antioxidant against oxidative stress induced by thyroid hormones overproduction during Basedow disease.