No abstract

No abstract

No abstract

No abstract

The TCN2 776C → G polymorphism is negatively associated with Alzheimer's type dementia, suggesting a protective role against the disease in subjects with the 5, 10-methylenetetrahydrofolate reductase 1298AA genotype.

Background/Aim: High serum levels of homocysteine and cortisol are independent risk factors for several pathologies and their levels can be regulated by some vitamins. Since the relationship between serum concentrations of homocysteine, cortisol and ascorbate has not been assessed in healthy individuals to date, it was the topic of the present work. Methods: The study group was composed of 20 men and 40 women aged >50 years. Blood samples were collected and serum concentrations of the analytes were quantified. Results: Serum homocysteine levels correlate positively with cortisol (r = 0.36, p <0.01) and age (r = 0.49, p < 0.001), and negatively with ascorbate (r = –0.30, p < 0.05) and folate (r = –0.31, p < 0.05). A negative correlation between serum levels of cortisol and ascorbate (r = –0.30, p < 0.05) was also observed. Multiple linear regression analysis showed that the best independent predictors of serum homocysteine concentration were cortisol (β = 0.319, p < 0.003), age (β = 0.529, p < 0.001) and folate (β = –0.338, p < 0.001). When subjects were divided into tertiles according to their homocysteine concentration, the highest tertile of homocysteine concentration has also higher cortisol (p < 0.005) and lower ascorbate (p < 0.05) concentrations compared with the lowest tertile of homocysteine concentration. Conclusion: The association between serum concentrations of homocysteine, cortisol and ascorbate suggests interaction between circulating levels of these molecules.

No abstract

Both adenosine A1 receptor and cGMP inhibit synaptic transmission at the hippocampus and recently it was found that A1 receptor increased cGMP levels in hippocampus, but the role of cGMP on A1 receptor-mediated inhibition of synaptic transmission remains to be established. In the present work we investigated if blocking the NOS/sGC/cGMP/PKG pathway using nitric oxide synthase (NOS), protein kinase G (PKG), and soluble guanylyl cyclase (sGC) inhibitors modify the A1 receptor effect on synaptic transmission. Neurotransmission was evaluated by measuring the slope of field excitatory postsynaptic potentials (fEPSPs) evoked by electrical stimulation at hippocampal slices. N6-cyclopentyladenosine (CPA, 15 nM), a selective A1 receptor agonist, reversibly decreased the fEPSPs by 54 ± 5%. Incubation of the slices with an inhibitor of NOS (L-NAME, 200 μM) decreased the CPA effect on fEPSPs by 57 ± 9% in female rats. In males, ODQ (10 μM), an sGC inhibitor, decreased the CPA inhibitory effect on fEPSPs by 23 ± 6%, but only when adenosine deaminase (ADA,1 U/ml) was present; similar results were found in females, where ODQ decreased CPA-induced inhibition of fEPSP slope by 23 ± 7%. In male rats, the presence of the PKG inhibitor (KT5823, 1 nM) decreased the CPA effect by 45.0 ± 9%; similar results were obtained in females, where KT5823 caused a 32 ± 9% decrease on the CPA effect. In conclusion, the results suggest that the inhibitory action of adenosine A1 receptors on synaptic transmission at hippocampus is, in part, mediated by the NOS/sGC/cGMP/PKG pathway.