Objective: To investigate whether exposure to the Chinese Famine in different life stages of early life is associated with cognitive functioning decline in adulthood.Methods: We recruited 1366 adults born between 1950 and 1964 and divided them into fetal-exposed, early childhood-exposed (1–3 years old during the famine), mid childhood-exposed (4–6 years old during the famine), late childhood-exposed (7–9 years old during the famine), and non-exposed groups. A selection of cognitive tests was administered to assess their cognitive performance. Association between malnutrition in different famine exposure periods and adult cognitive performance was estimated by multivariate logistic and multiple linear regression analyses.Results: There were significant differences in cognitive performance between subjects exposed to famine during different life stages. For the general cognitive tests, fetal-exposed period was associated with decreased scores of the Mini-Mental State Examination (MMSE), and late childhood-exposed with decreased scores of the Montreal Cognitive Assessment (MoCA). We also found exposure to famine during mid and late childhood was associated with worse performance on the Stroop color and word test.Conclusion: Famine exposure in utero and during childhood is associated with overall and specific cognitive decline, affecting selective attention and response inhibition particularly.

BackgroundTo investigate the relationship between oxysterols and mild cognitive impairment (MCI) in a matched case–control study.MethodsThe plasma levels of four oxysterols, 27–hydroxycholesterol (27–OHC), 24S–hydroxycholesterol (24S–OHC), 7α–hydroxycholesterol (7α–OHC) and 7β–hydroxycholesterol (7β–OHC), were analyzed by High Performance Liquid Chromatography–Mass Spectrometry (HPLC–MS) and compared between 70 MCI patients and 140 matched controls with normal cognition. The odds ratio (OR) was calculated using logistic analyses to assess the association between oxysterols and MCI.ResultsCompared with controls with normal cognition, plasma level of 27–OHC was significantly higher in MCI patients. Logistic analyses suggested high plasma level of 27–OHC was significantly associated with MCI even after multivariate adjustment (OR = 2.86, 95 % CI: 1.52 ~ 5.37).ConclusionsOur findings suggested that the increased plasma level of 27-OHC was associated with MCI, suggesting high plasma levels of 27-OHC may pay an important role in the development of MCI.

This study indicates that the mechanisms of dietary cholesterol on learning and memory impairment may be involved in cholesterol metabolism and lysosome function with the increase of plasma 27-OHC, thus resulting in Aβ formation and accumulation.

The aim of the present study was to investigate the effects of diet cholesterol on oxysterol levels and amyloid‑β (Aβ) production in the peripheral blood and the brains of Sprague‑Dawley (SD) rats. SD rats were randomly divided into five groups and fed 0.015, 0.05, 0.2, 0.5 and 1.6% cholesterol‑containing diets for 8 weeks. The effect of the different diets on the levels of cholesterol, oxysterols [including 27‑hydroxycholesterol (OHC), 24S‑OHC, 7α‑OHC and 7β‑OHC], and the Aβ1‑40 and Aβ1‑42 peptides were examined in the plasma and the brain of the rats. The results demonstrated that diet cholesterol increased the levels of plasma cholesterol in a dose‑dependent manner. The plasma levels of 27‑OHC, 7α‑OHC and 7β‑OHC significantly increased in the 0.5 and 1.6% cholesterol diet groups and the brain levels of 27‑OHC significantly increased in the 1.6% cholesterol diet group. Increased concentration of cholesterol in the diet had no significant influence on plasma and brain levels of 24S‑OHC in the rats. In addition, Aβ1‑40 and Aβ1‑42 levels in plasma and brain were significantly elevated following administration of 0.5 and 1.6% diet cholesterol. The present study revealed that high diet cholesterol contributed to increased level of oxysterols, especially 27‑OHC, in the peripheral blood and the brain, which may be the link between increased peripheral cholesterol and brain Aβ production.

BackgroundIt was reported that Glutathione S-transferase (GST) gene polymorphism and fruit and vegetable (FV) intake were associated with body antioxidant capacity. The oxidative/anti-oxidative imbalance played an important role in the pathogenesis of AD. However, the association of GST genotype, dietary FV consumption with body antioxidant biomarkers and cognitive function in the elderly is not clear.ObjectiveThe aim of the present study was to determine the association of GST genotype, and dietary FV intake, with antioxidant biomarkers and cognitive function in the elderly.MethodsFood frequency questionnaire was used to collect data of dietary FV intakes in 504 community dwelling elderly aged from 55 to 75 years old. GSTM1 and GSTT1 genotypes were determined by using multiple-PCR method. Plasma and erythrocyte antioxidant biomarkers were measured. Cognitive function was measured by using Montreal Cognitive Assessment. Statistical analysis was applied for exploring the association of GST genotype and FV intake with antioxidant biomarkers level and cognitive function in the elderly.ResultsIndividual GSTM1 or GSTT1 gene deletion affects body antioxidant biomarkers levels, including erythrocyte GST activity, plasma total antioxidant capacity, and glutathione levels. GSTM1and/or GSTT1 gene deletion have no effects on cognitive function in the surveyed participants. The effect of GST genotype on antioxidant biomarkers are FV intake dependent. There is interaction of FV intake and GST genotype on cognitive function in the elderly.ConclusionGST genotype or daily FV consumption impact body antioxidant biomarkers, but not cognitive function in the elderly. There were combined effects of GST genotype and FV consumption on cognitive function in the elderly population. Large scale perspective population study is required to explore the association of GST genetic polymorphism, FV consumption and antioxidant biomarkers and cognitive function in the elderly.