(c) 2009 Elsevier Ireland Ltd All rights reserved “
“Person

(c) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Persons with Down syndrome show an altered immune response and an increased susceptibility to Alzheimer’s disease. In a prospective study, we examined whether the plasma neopterin level, a marker for cell-mediated immune activation and inflammation, is associated with an increased risk of dementia in persons with Down syndrome. Plasma concentrations of neopterin were determined in a population-based study of 394 persons with Down syndrome, who were screened

annually for dementia. We used Cox proportional hazards model to determine risk of dementia. Demented persons with Down syndrome have a significantly (p=0.05) higher plasma neopterin concentration than the non-demented. In the non-demented without autoimmune disorders, in those with a plasma level of neopterin above median, the risk to develop LCL161 concentration dementia increased to 1.83 (95% confidence interval: 1.04-3.20). High plasma neopterin selleck chemicals level is an independent determinant of the risk of dementia in persons with Down syndrome. (c) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Nicotine addiction in women increases the risk of ischemic stroke. Importantly, women who smoke and use hormone replacement therapy/oral contraceptives greatly increase their risk of coronary heart disease and ischemic stroke as compared to nonsmoking women who use occasionally

oral contraceptives. Nicotine addiction disturbs the normal periodicity of the menstrual cycle and induces early onset of menopause in women; however, the mechanism of the synergistic effects of nicotine and sex hormones on cerebrovascular health is not clearly understood. In the current study based on a rat model of global cerebral ischemia, our goals are (1) to determine whether

chronic nicotine exposure abrogates beneficial effects of estrogen on hippocampal neurons subjected to ischemia, and (2) to determine whether nicotine exposure antagonizes estrogen signaling by reducing U0126 the availability of estrogen receptor(s). To test the effects of chronic nicotine exposure, normally cycling or ovariectomized rats were injected with nicotine daily for 15 days. To investigate the efficacy of estrogen treatment, nicotine-exposed ovariectomized rats were injected with a bolus of 17 beta-estradiol and 48 h later ischemia was induced. Our results demonstrated that chronic nicotine exposure followed by ischemic insult at the proestrus stage of the estrous cycle showed that only 14% of normal neurons remained compared to the non-nicotine-treated group (p < 0.05). Similarly, a bolus of 17 beta-estradiol to nicotine-treated ovariectomized rats showed only 26% of normal neurons remaining as against 47% in the non-nicotine-treated group. Nicotine exposure decreased ER(3 but not ER alpha protein levels in the hippocampus, suggesting a role for ER beta in increased post-ischemic neurodegeneration from nicotine exposure.

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