Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Early life adversity (ELA) tends to accelerate neurobiological ageing, which, in turn, is thought to heighten vulnerability to both major depressive disorder (MDD) and Alzheimer’s disease (AD). The two conditions are putatively related, with MDD representing either a risk factor or early symptom of AD. Given the substantial environmental susceptibility of both disorders, timely identification of their neurocognitive markers could facilitate interventions to prevent clinical onset. To this end, we analysed multimodal data from the Adolescent Brain and Cognitive Development study (ages 9–10 years). To disentangle genetic from correlated genetic-environmental influences, while also probing gene-adversity interactions, we compared adoptees, a group generally exposed to substantial ELA, with children raised by their biological families via genetic risk scores (GRS) from genome-wide association studies. AD and MDD GRSs predicted overlapping and widespread neurodevelopmental alterations associated with superior fluid cognition. Specifically, among adoptees only, greater AD GRS were related to accelerated structural maturation (i.e., cortical thinning) and higher MDD GRS were linked to delayed functional neurodevelopment, as reflected in compensatory brain activation on an inhibitory control task. Our study identifies compensatory mechanisms linked to MDD risk and highlights the potential cognitive benefits of accelerated maturation linked to AD vulnerability in late childhood.
Early life adversity (ELA) tends to accelerate neurobiological ageing, which, in turn, is thought to heighten vulnerability to both major depressive disorder (MDD) and Alzheimer’s disease (AD). The two conditions are putatively related, with MDD representing either a risk factor or early symptom of AD. Given the substantial environmental susceptibility of both disorders, timely identification of their neurocognitive markers could facilitate interventions to prevent clinical onset. To this end, we analysed multimodal data from the Adolescent Brain and Cognitive Development study (ages 9–10 years). To disentangle genetic from correlated genetic-environmental influences, while also probing gene-adversity interactions, we compared adoptees, a group generally exposed to substantial ELA, with children raised by their biological families via genetic risk scores (GRS) from genome-wide association studies. AD and MDD GRSs predicted overlapping and widespread neurodevelopmental alterations associated with superior fluid cognition. Specifically, among adoptees only, greater AD GRS were related to accelerated structural maturation (i.e., cortical thinning) and higher MDD GRS were linked to delayed functional neurodevelopment, as reflected in compensatory brain activation on an inhibitory control task. Our study identifies compensatory mechanisms linked to MDD risk and highlights the potential cognitive benefits of accelerated maturation linked to AD vulnerability in late childhood.
We investigated the effects of fermented rice bran (FRB) administration in two groups of C57BL/6J mice. The first group was fed with a high-fat diet, and the second group was fed with a high-fat diet supplemented with the FRB for 8 weeks. FRB supplementation suppressed the high-fat-induced weight gain and considerable alterations in the intestinal microbiota profile in the second group. Among 27 bacterial genera detected in the FRB, only Enterococcus, Lactobacillus, Bacteroides, Prevotella, and the unclassified family Peptostreptococcaceae were detected in mice feces. Their abundances were not particularly increased by FRB supplementation. The abundances of Enterococcus and the unclassified family Peptostreptococcaceae were even suppressed in the second group, suggesting that FRB supplementation didn't cause an addition of beneficial microbiome but inhibit the proliferation of specific bacteria. Fecal succinic acid concentration was significantly decreased in the second group and highly correlated with the relative abundances of Turicibacter, Enterococcus, and the unclassified family Peptostreptococcaceae. A significant increase in fumaric acid and a decrease in xylitol, sorbitol, uracil, glutamic acid, and malic acid levels were observed in the peripheral blood of the second group. FRB supplementation counteracted the high-fat-induced obesity in mice by modulating the gut microbiota and the host metabolism.
ObjectiveThere is a lack of risk factors that can effectively identify gestational diabetes mellitus (GDM) in early pregnancy. It is unclear whether serum taurine in the first trimester and dynamic changes have different characteristics in GDM women. Whether these features are associated with the occurrence of GDM has not yet been elucidated. The main objective of this study was to observe the dynamic changes of serum taurine during pregnancy and investigate the relationship between serum taurine levels and GDM in the first and second trimesters.MethodsThis was a nested case-control study in 47 women with GDM and 47 age-matched normoglycemic women. We examined serum taurine at 8-12 weeks’ gestation and 24-28 weeks’ gestation. The serum taurine of the two groups was compared. Multivariable logistic regression analysis was performed to investigate how serum taurine was associated with GDM.ResultsThe serum taurine concentration of GDM women was significantly lower than that of normoglycemic women in the first trimester(2.29 vs 3.94 μmol/L, P<0.001). As the pregnancy progressed, serum taurine concentration in normoglycaemic women decreased significantly(3.94 vs 2.47 μmol/L, P<0.001), but not in the GDM group(2.29 vs 2.37 μmol/L, P=0.249), resulting in the disappearance of differences between the two groups(2.47 vs 2.37 μmol/L, P=0.160). After adjustment for pre-pregnancy body mass index(BMI), fasting plasma glucose(FPG), and lipid profiles in the first trimester, the serum taurine concentration in the first trimester was negatively correlated with the risk of GDM(OR=0.017, 95% CI=0.003-0.107, P<0.001). Furthermore, dynamic change of serum taurine showed a significantly positive correlation with the risk of GDM(OR=9.909, 95% CI=3.556-27.610, P<0.001).ConclusionLow serum taurine concentration in the first trimester was significantly associated with the development of GDM. As the pregnancy progressed, the association between serum taurine and GDM disappeared in the second trimester, which might be related to the inhibition of taurine transporter(TauT) activity by high glucose.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.