Polymorphism of MTHFR C677T, serum vitamin levels and cognition in subjects with hyperhomocysteinemia in China.

Relationships between hyperhomocysteinemia (HHE) and neurodegenerative diseases have been widely studied. However, the impact of serum total homocysteine (tHcy) levels on cognitive function has not been confirmed. C677T polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have impacts on tHcy level; it is suspected to influence cognitive function, but only few investigations have assessed its effects on non-dementia adults and the results have been controversial. Moreover, there is no report about Chinese subjects. In the present study, we determined C677T/MTHFR genotype, serum tHcy concentration and cognition in 182 nondemented subjects aged 55-88 years to probe the associations between MTHFRC677T mutation, increased tHcy levels and decreased cognitive function in a northern city in China. A serum tHcy level > or = 16 micromol/l was deemed HHE. Cognitive function was assessed by the Mini Mental State Examination (MMSE) and Basic Cognitive Aptitude Tests (BCAT). Results showed that: (i) subjects with the T allele had higher serum tHcy levels than those without, especially in lower folate status; (ii) T allele and CT/TT genotype frequencies in subjects with HHE were higher than in non-HHE subjects (P < 0.05); and (iii) serum tHcy level was inversely related to total BCAT score (P < 0.05) but MTHFR677 C to T polymorphism had no association with it. Our results confirmed that the MTHFR 677 C to T mutation, especially in lower serum folate concentration status, results in the increase of serum tHcy levels which is bad for cognitive function and indicates that higher serum folate level is of benefit in keeping lower serum tHcy level and better cognitive function. The results provide some valuable clues for individualized nutrition intervention of HHE and cognition decline in the middle-aged and the elderly.

[Cytoprotective effect of blueberry extracts against oxidative damage of rat hippocampal neurons induced by H2O2].

OBJECTIVE: To investigate the protective effect of blueberry extract (BE, 25% anthocyanins) against oxidative damage in primary cultures of rat hippocampal neurons induced by H2O2. METHODS: Rat hippocampal neurons were randomly assigned to control group, H2O2 group and BE pretreatment groups, BE at six different doses (0.01, 0.1, 1.0, 10.0, 20.0 and 40 microg/ml) and then exposed to 50 micromol/L H2O2 for twenty-four hours. To selecte the most fittest concentration of BE by testing viability of neurons and activity of LDH. Then MDA concentration, SOD activity and neuronal apoptosis were(checked) measured. RESULTS: (1) Compared with H2O2 group, the hippocampal cell viabilities in the 0.1, 1.0 and 10 microg/ml BE groups were significantly increased from 57.44% to 78.42%, 87.71% and 72.40% separately. The activity of LDH in BE groups at varied concentrations (0.1, 1.0 and 10 microg/ml) was significiantly lower than that in H2O2 group. It was found that 1 microg/ml BE had the furthest protective effect against oxidative damage in primary cultures of rat hippocampal neurons induced by H2O2. (2) The concentration of MDA and the rate of neuronal apoptosis of BE group (1 microg/ml) were much lower than H2O2 group, while SOD activity was much higher. CONCLUSION: Proper dose of BE has remarkable protective effect against oxidative stress in primary cultures of rat hippocampal neurons induced by H2O2, the mechanism may be related to decreasing the neuronal apoptosis and enhancing the antioxidation of hippocampal neurons.