Effects of Quercetin Intervention on Cognition Function in APP/PS1 Mice was Affected by Vitamin D Status.

SCOPE: To explore how quercetin will affect memory impairments in APP/PS1 mice under different vitamin D status. METHODS AND RESULTS: APP/PS1 mice are divided into four groups, i.e., control (CON), low (LVD), medium, and high vitamin D supplemented with quercetin. During Morris Water Maze test, mice of the LVD group function best for improving cognitive function demonstrated by reduced latency to platform, and increased number of crossing and swimming distance in the target quadrant. Compared to the CON group, in both hippocampus and cortex, the LVD group has significant reduction in Aß plaques, p-Tau at Ser396&Ser404, and neuroinflammation. In the hippocampus, BDNF is elevated, miR-26a and miR-125b is decreased, while miR-132 is increased in the LVD group. The LVD group demonstrates increased gut microbial diversity and elevated relative abundance of Glutamicibacter, Facklamia and Aerocorrus. In the hippocampus, p-Tau at ser396&404, GFAP, Ibα1, miR-26a, and miR-132 are negatively correlated with Aerococcus; and p-Tau at ser404 and Ibα1 are negatively correlated with Facklamia. CONCLUSION: Quercetin is more efficacious for improving cognitive function under low vitamin D status. This might be owing to that interventions reduce Aß plaques, tau phosphorylation, and neuroinflammation, upregulate BDNF, reduce miR-26a and miR-125b, increase miR-132, and elevate gut microbial diversity including Facklamia and Aerococcus.

Chia Seed Does Not Improve Cognitive Impairment in SAMP8 Mice Fed with High Fat Diet.

BACKGROUND: Chia seed is an ancient seed with the richest plant source of α-linolenic acid, which has been demonstrated to improve metabolic syndrome associated risk factors. Under high fat diet (HFD) condition, the senescence-accelerated mouse-prone 8 (SAMP8) mice demonstrated worsen Alzheimer's disease (AD) related pathology compared to low fat diet fed SAMP8 mice. OBJECTIVE: To explore whether chia seed supplementation might improve cognitive impairment under aging and metabolic stress via high fat diet (HFD) fed SAMP8 mice as a model. DESIGN: SAMP8 mice and senescence-accelerated mouse-resistant 1 (SAMR1) were randomized into 4 groups, i.e., SAMR1 low fat diet group (SAMR1-LFD), SAMP8-HFD and SAMP8-HFD group supplemented with 10% chia seed (SAMP8-HFD+Chia). At the end of the intervention, cognitive function was measured via Morris water maze (MWM) test. Hippocampus and parietal cortex were dissected for further analysis to measure key markers involved AD pathology including Aß, tau and neuro-inflammation. RESULTS: During navigation trials of MWM test, mice in SAMP8-LFD group demonstrated impaired learning ability compared to SAMR1-LFD group, and chia seed had no effect on learning and memory ability for HFD fed SAMP8 mice. As for Alzheimer's disease (AD) related pathology, chia seed not only increased α-secretase such as ADAM10 and insulin degrading enzyme (IDE), but also increased ß-secretase including beta-secretase 1 (BACE1) and cathepsin B, with an overall effects of elevation in the hippocampal Aß42 level; chia seed slightly reduced p-Tauser404 in the hippocampus; while an elevation in neuro-inflammation with the activation of glial fibrillary acidic protein (GFAP) and Ibα-1 were observed post chia seed supplementation. CONCLUSIONS: Chia seed supplementation did not improve cognitive impairment via MWM in HFD fed SAMP8 mice. This might be associated with that chia seed increased key enzymes involved both in non-amyloidogenic and amyloidogenic pathways, and neuro-inflammation. Future studies are necessary to confirm our present study.

Reproductive factors and risk of Parkinson's disease in women: A meta-analysis of observational studies.

Evidence on the relationship between reproductive factors, use of oral contraceptives (OCs) and the incidence of Parkinson's disease (PD) remain inconclusive. The aim of this meta-analysis is to evaluate whether relevant reproductive factors including age at menarche, age at menopause, fertile lifespan, parity, type of menopause (surgical versus natural), and use of OCs are associated with risk of PD in women via random-effects model. PubMed and EMBASE database were used to search for case-control or cohort studies published before February17, 2017. 6 case-control and 5 cohort studies were included in the meta-analysis. The pooled relative risks (RRs) of PD risk were 1.00 (95% CI: 0.79-1.28) for use of OCs (ever versus never), 1.03 (95% CI: 0.84-1.26) for age at menarche, 0.98 (95% CI: 0.75-1.29) for age at menopause, 0.98(95% CI: 0.77-1.25) for fertile lifespan, 0.99(95% CI:0.0.79-1.25) for parity, 0.93 (95% CI:0.68-1.29) for type of menopause (surgical versus natural). In the subgroup analysis stratified by study design, age, caffeine intake and smoking, an inverse association was found between surgical menopause and risk of PD for those adjusting for caffeine intake (RR: 0.67, 95% CI: 0.45-0.99) and smoking (RR: 0.77, 95% CI: 0.63-0.94); while a positive association was found between surgical menopause and PD risk for those not adjusting for smoking (RR: 1.91, 95% CI: 1.29-2.83). In conclusion, our meta-analysis provided little epidemiological support for the role of reproductive factors in the incidence of PD. Whether surgical menopause is inversely associated with the risk of PD requires further explorations.