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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.

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Adenosine A1 and cannabinoid CB1 receptors are highly expressed in hippocampus where they trigger similar transduction pathways. We investigated how the combined acute activation of A1 and CB1 receptors modulates cAMP accumulation in rat hippocampal slices. The CB1 agonist WIN55212-2 (0.3–30 μM) decreased forskolin-stimulated cAMP accumulation with an EC50 of 6.6 ± 2.7 μM and an E max⁡ of 31% ± 2%, whereas for the A1 agonist, N6-cyclopentyladenosine (CPA, 10–150 nM), an EC50 of 35 ± 19 nM, and an E max⁡ of 29% ± 5 were obtained. The combined inhibitory effect of WIN55212-2 (30 μM) and CPA (100 nM) on cAMP accumulation was 41% ± 6% (n = 4), which did not differ (P > 0.7) from the sum of the individual effects of each agonist (43% ± 8%) but was different (P < 0.05) from the effects of CPA or WIN55212-2 alone. Preincubation with CPA (100 nM) for 95 min caused desensitization of adenosine A1 activity, which did not modify the effect of WIN55212-2 (30 μM) on cAMP accumulation. In conclusion, the combined effect of CB1 and A1 receptors on cAMP formation is additive and CB1 receptor activity is not affected by short-term A1 receptor desensitization.