Background: Oral supplementation of anserine/carnosine helps preserve cognitive functions in healthy older adults. Mild cognitive impairment (MCI) is a transition between cognitive-normal and dementia. Therefore, it needs to investigate whether anserine/carnosine supplementation (ACS) has effects on subjects with MCI. Methods: A randomized, double-blind, placebo-controlled 12-week trial was performed. Fifty-four subjects with MCI were randomized to an active group ingesting 750 mg of anserine and 250 mg of carnosine per day or a placebo (1:1). Evaluation of cognitive change was conducted utilizing a psychometric test battery. Results: The score improvement in the global Clinical Dementia Rating (gloCDR) was superior in the active group than placebo (p = 0.023). No beneficial effect in the active group was detected in the other psychometric tests including the Mini-Mental State Examination (MMSE), the Wechsler Memory Scale, and the Alzheimer’s Disease Assessment Scale (ADAS). When APOE4 positive (APOE4 (+)) or negative (APOE4 (-)) subjects were separately analyzed, beneficial change in the APOE4 (+) subjects was observed in MMSE (p = 0.025) as well as in gloCDR (p = 0.026). Conclusions: The present study might suggest that protective effects against cognitive decline in APOE4 (+) MCI subjects exist.

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The Ets family transcription factor PU.1 is required for the development of various lymphoid and myeloid cell lineages, and regulates the expression of several genes in a cell type-speci¢c manner. Recently we found that overproduction of PU.1 in mouse bone marrow-derived mast cell progenitors induced the expression of monocyte-speci¢c genes. This prompted us to analyze the functions of each domain of PU.1 in monocyte-speci¢c gene expression, using transfection of mast cell progenitors with a series of retrovirus vectors for overexpression of various truncation mutants. Both the acidic region and the Ets domain of PU.1 were required for expression of monocyte-speci¢c genes, and for enhanced interleukin-6 production in response to lipopolysaccharide. The Gln-rich region was suggested to be involved in expression of both MHC class II and F4/80. On the other hand, when PU.1 protein lacking the PEST domain was produced in the progenitor cells, expression of monocyte-speci¢c genes was substantially enhanced, suggesting that the PEST domain plays a negative role in monocyte-speci¢c gene expression.

Matcha Green Tea Powder contains a variety of active ingredients beneficial to health, such as tea catechins, lutein and vitamin K. It is also known that these ingredients confer benefits upon cognitive functions of elderly people. Therefore, we aimed to investigate the relationship between a daily supplementation of Matcha and the change in cognitive functions of community-dwelling elderly people. A randomized, double-blind, placebo-controlled 12-week trial was performed. Sixty-one participants were recruited and randomly assigned to receive test drink containing 3 g powder from fresh Matcha or placebo powder per day. Changes in cognitive function were assessed utilizing a psychometric test battery. Daily food intake was assessed by a Brief-type Self-administered Diet History Questionnaire (BDHQ). In the gender-specific analysis, a significant cognitive enhancement was observed in the Montreal Cognitive Assessment (MoCA) score in the active group of women. In dietary analysis, we found a significant inverse correlation between consumption of vitamin K in daily diet, excluding test drinks, and change in MoCA. The present study suggests that daily supplementation of Matcha Green Tea Powder has protective effects against cognitive decline in community-dwelling elderly women.

BackgroundThe effect of the interaction between long-term mental stress and eating habits on weight gain has not been confirmed in humans.MethodsA population of 1080 healthy Japanese male local government employees without lifestyle-related diseases were studied. Height and weight were measured and perception of mental stress and the frequency of eating to satiety, drinking, smoking, and exercise were surveyed by means of a questionnaire in both 1997 and 2002. Exposure patterns during this 5-year period were classified as low or high. Information on daily food and energy intake was collected in 2002. The effect of the interaction between stress and the frequency of eating to satiety on change in BMI (ΔBMI) during this 5-year period was examined by 2-way analysis of variance (ANOVA) and covariance (ANCOVA) adjusted for age, BMI at baseline, and other lifestyle habits. The association between satiation eating and ΔBMI was compared between participants with high and low levels of stress.ResultsStress and satiation eating were not significantly mutually correlated. Two-way ANCOVA showed a significant interaction (F = 4.90, P = 0.03) between mental stress and satiation eating. Among participants with a high level of stress, BMI gain was significantly larger in those who ate to satiety than in those who ate moderately, when ΔBMI was unadjusted or adjusted for covariates (adjusted mean [SE]: 0.34 ± 0.06 kg/m2 vs. 0.12 ± 0.07 kg/m2, P = 0.002). Among participants with a low level of stress no such difference was observed. These results were unchanged after further adjustment for energy intake in 2002.ConclusionIn this population, eating pattern interacted with long-term mental stress to produce a larger body mass gain in satiation eaters than in moderate eaters among participants with a high level of stress, independent of energy intake or other lifestyle habits.