Nutritional Neuroscience最新文献

Objectives: Babassu coconut (Orbignya phalerata) is an important economic and nutritional resource for many rural communities in Brazil. Babassu oil (BO) contains low levels of essential fatty acids (EFAs), which are crucial nutrients for physical and neurological development. However, it remains unclear whether BO consumption can affect these aspects. We investigated somatic maturation, reflex ontogeny, anxiety-like behavior, and brain susceptibility to cortical spreading depression (CSD) in the offspring of rat dams fed a BO-diet.

Methods: Wistar dams were fed diets containing either BO or soybean oil (control) during gestation and lactation. After weaning, pups either continued their mothers' diets or switched to the control diet. Offspring were analyzed during adolescence (groups Soy and Bab, n = 64) or adulthood (groups Soy-Soy, Bab-Bab and Bab-Soy, n = 26).

Results: Compared to controls, the Bab group showed developmental delays in reflex ontogeny (palmar grasp, cliff avoidance, and negative geotaxis, p < 0.05) and somatic maturation (ear unfolding, superior teeth eruption, eye opening, and ear opening, p < 0.05). At both ages, anxiety-like behavior (elevated-plus maze) did not differ between groups. For CSD, the Bab (adolescent) and Bab-Bab (adult) groups exhibited higher and lower CSD velocities, respectively, compared to age-matched controls (p < 0.001). This effect was not reversed in the Bab-Soy group.

Discussion: We suggest that BO consumption during pregnancy and lactation should be considered with caution, as it may pose premature and long-term risks to neurodevelopment and cortical excitability.

Background: The global incidence of obesity and metabolic disorders has been associated with alterations in the central nervous system, prominently featuring increased oxidative stress and heightened production of amyloid beta peptide (AB), stemming from mitochondrial dysregulations, which potentially contribute to the onset of neurodegenerative disorders like Alzheimer disease.

Aims: In this study, we sought to ascertain whether chronic consumption of unbalanced diets by rats leads to elevated AB production and accumulation in brain structures, driving neuronal damage and mitochondrial dysfunction.

Methods: Male Wistar rats were fed with unbalanced diets rich in sucrose or lard for 12 months. Subsequently, we evaluated zoometric and biochemical parameters, including glucose tolerance, serum cholesterol, and triglycerides, alongside spatial memory. Additionally, AB accumulation, oxidative stress markers, and mitochondrial respiratory chain activity were analyzed in mitochondria and homogenates from the hippocampus and cerebral cortex.

Results: In our results, both dietary interventions induced abdominal obesity and spatial memory deterioration, associated to glucose metabolism disturbance, mitochondrial dysfunction, and increased oxidative stress. Nevertheless, AB accumulation was evident only in the mitochondria of rats fed with the sucrose-enriched diet.

Conclusions: With these findings, we show that, although excessive consumption of fat or sucrose drives to obesity, only the last could potentially bridge the gap between obesity and neurodegenerative pathogenesis, thereby highlighting the relevance of lifestyle and diet quality, bringing a way to develop preventive strategies.

Objectives: As extensively researched metabolites, short chain fatty acids (SCFAs) undergo significant alterations in individuals with Parkinson's disease (PD). This meta-analysis was conducted to (1) explore the relationship between SCFAs and PD, and (2) provide evidence for the metabolic mechanisms underlying PD pathogenesis.

Methods: A systematic search of four electronic databases (PubMed, Embase, Web of Science and Cochrane Library) was conducted up to February 29, 2024. The Agency of Healthcare Research and Quality (AHRQ) criteria were used for quality evaluation. Forest plots were used to display the results of the meta-analysis, and publication bias was assessed using funnel plots, Begg's tests and Egger's tests. Sensitivity analysis revealed heterogeneous sources among the included studies.

Results: A total of 9 independent studies were enrolled, including 485 PD patients and 338 controls. In this meta-analysis, we discovered that, in comparison to healthy controls, stool acetic (SMD: -0.80; 95% CI: -1.23, -0.37), butyric (SMD: -0.71; 95% CI: -1.19, -0.24) and propionic acids (SMD: -0.98; 95% CI: -1.57, -0.40) were decreased, while plasma butyric (SMD: 0.25; 95% CI: 0.05, 0.44), isobutyric (SMD: 0.35, 95% CI: 0.11, 0.59) and propionic acids (SMD: 0.37, 95% CI: 0.16, 0.58) were increased in PD patients. Other SCFAs were not significantly different between the two groups.

Conclusions: The evidence from this meta-analysis demonstrates that the stool and plasma SCFAs of PD patients are distinct from those of the control group. This study highlights SCFAs' potential importance as novel interventional targets.

Objective: This study aims to investigate the protective effect and underlying mechanism of Saikosaponin A (SSA) against oxidative stress-induced damage in mouse cochlear hair cells (HEI-OC1).

Methods: An oxidative stress model was established by treating HEI-OC1 cells with 50 mU/mL glucose oxidase (GO). Cells were divided into four groups: Control, GO, Control + SSA, and GO + SSA (1 μM SSA). Cell viability was assessed using the CCK-8 assay, and apoptosis was evaluated by flow cytometry and by analyzing expression of BAX, BCL-2, and cleaved CASPASE-3. Oxidative stress levels were assessed via malondialdehyde (MDA), reactive oxygen species (ROS), and glutathione peroxidase (GSH-Px). mRNA levels of Ptgs2 (COX-2), Nos2 (iNOS), Hmox1 (HO-1), and Sod1 (SOD1) were detected by qRT-PCR. Protein expression of KEAP1, NFE2, and phosphorylated NFE2 was examined by western blot, including analysis of nuclear translocation. All experiments were independently performed in triplicate.

Results: SSA increased cell viability by approximately 40% (P < 0.01) and reduced apoptotic rate by 70% (P < 0.001) in GO-treated HEI-OC1 cells. SSA also decreased MDA and ROS levels and restored GSH-Px activity (P < 0.01). Moreover, SSA downregulated Ptgs2 and Nos2 expression, while upregulating Hmox1 and Sod1. At the protein level, SSA suppressed KEAP1 expression, enhanced NFE2 and p-NFE2 levels, and promoted NFE2 nuclear translocation.

Conclusion: SSA alleviates GO-induced oxidative stress and apoptosis in HEI-OC1 cells by activating the KEAP1/NFE2 signaling pathway. These findings support the potential application of SSA in protecting cochlear hair cells from oxidative damage, warranting further in vivo investigation.

Objective: Depression is a global health issue, with traditional antidepressants raising safety concerns. Indian mustard honey (MH) offers a potential alternative due to its health benefits, though its antidepressant effects remain unexplored. This study investigates the neuroprotective and antidepressant effects of MH in HT-22 cells in vitro and in Wistar rats in vivo.

Methods: Chemical constituents of MH were identified using liquid chromatography-mass spectrometry (LC-MS). Effects of MH on phosphorylated tyrosine kinase receptor B (p-TrkB), brain-derived neurotropic factor (BDNF) and phosphorylated cyclic AMP-dependent response element-binding protein (p-CREB) were assessed in reserpine-treated HT-22 cells and rat models. Antidepressant effects in rats were evaluated using forced swim, tail suspension and locomotor activity tests, along with hippocampal histopathology and molecular analyses.

Results: MH profiling identified key polyphenols with antioxidant properties. In HT-22 cells, MH showed neuroprotection at 60 mg/mL (p < 0.001), and upregulated p-TrkB, BDNF, and p-CREB (p < 0.001) against reserpine-induced oxidative stress. In rats, compared to fluoxetine, MH at 1 g/kg BW increased locomotor activity by ∼2.3 fold and reduced immobility by ∼50% and 25% in the tail suspension and forced swim tests (p < 0.001), respectively, showing comparable/ better antidepressant effects. It also preserved hippocampal architecture and upregulated p-TrkB, BDNF, and p-CREB (p < 0.001) levels compared to reserpine-treated rats.

Discussions: MH demonstrated antioxidant, neuroprotective and antidepressant activities in in vitro and in vivo models, suggesting therapeutic potential. However, further studies on additional pathways, including β-catenin/Wnt, MAPK/ERK, along with pharmacokinetics, are essential before recommending MH as an antidepressant agent.

Objective: This study explores the relationship between Mild Cognitive Impairment (MCI), mood disturbances, and tryptophan (TRP) metabolites of the kynurenine and serotonin pathway in older adults, focusing on the acute effects of a TRP-rich protein meal.

Methods: 32 older adults (age 55 and up) with MCI (MoCA score 18-26) and 26 older adults without MCI matched for age, sex, and body mass index (BMI) were assessed for mood and TRP metabolites. A subset of these subjects then consumed an alpha-lactalbumin (ALAC) meal rich in TRP. Plasma TRP metabolite concentrations and mood (using the Profile of Mood States (POMS) scale) were assessed before and 3 h after intake.

Results: At baseline, MCI subjects had higher plasma anthranilic acid than non-MCI controls (p = 0.015). Intake of ALAC resulted in increases in plasma TRP, kynurenine, 3-hydroxykynurenine, kynurenic acid, picolinic acid (all p < 0.001), and anthranilic acid (p = <0.001) but not in serotonin (p = 0.065). Higher picolinic acid levels were found after ALAC intake in the MCI than in the non-MCI group (p = <0.001). The TRP/large neutral amino acid ratio increased by 89.9% in MCI subjects and 95.9% in controls. There were no acute changes in mood after ALAC intake.

Discussion: Older adults with MCI showed elevated baseline anthranilic acid, and TRP-rich protein intake acutely increases TRP availability and upregulates the kynurenine but not serotonin pathway without mood improvement. Post-ALAC increases in picolinic acid in MCI subjects warrants further investigation.Trial registration: ClinicalTrials.gov identifiers: NCT05395390, NCT02082418.

Several population-based studies suggest that dietary creatine may benefit depression and cognitive function, but no research has examined overall mental health in a non-U.S. population or included adolescents. This cross-sectional study investigated the relationship between daily creatine consumption and mental health indicators using data from the 2022 Korean National Health and Nutrition Examination Survey (KNHANES). Data were analyzed from 5,257 individuals (56% female, mean age 51.1 ± 19.0 years) who provided dietary intake information and completed at least one mental health assessment. The mean daily creatine intake was 10.3 ± 9.5 mg/kg body mass (95% CI, 10.0 -10.5). One-way ANOVA showed significant differences in depression scores across quartiles of creatine intake (F = 4.003, p = 0.007), with higher depression scores in the lowest quartile compared to all others (p ≤ 0.05). The prevalence of depression was greatest among participants in the lowest quartile (6.9%) versus Q2 (3.3%), Q3 (4.3%), and Q4 (3.6%) (p≤0.05). Participants in the lowest quartile also reported higher rates of suicidal thoughts, plans, and attempts compared to those in higher quartiles (p ≤ 0.05). Higher creatine intake was associated with lower odds of generalized anxiety disorder after controlling for biomarkers of creatine turnover and demographic variables (p ≤ 0.05), but this relationship was not significant when lifestyle factors were included (p > 0.05). These findings suggest that higher dietary creatine intake may have modest protective effects against depression, suicidality, and anxiety. However, given the cross-sectional design, causality cannot be inferred, and further longitudinal and interventional studies are needed to confirm these associations and explore underlying mechanisms.

Ischemia is a condition occured when there is insufficient blood flow to the tissues, negatively affecting cellular energy production. Brain ischemia is a critical pathological process caused neuronal function to deteriorate and cell death due to the temporary or permanent interruption of cerebral blood circulation. During this process, triggering endoplasmic reticulum (ER) stress disrupts intracellular protein folding mechanisms, leading to increased neuronal damage. This study investigated the effect of a 1-week supplementation with 3',4'-Dihydroxyflavonol (DiOHF) on endoplasmic reticulum stress in cerebellum tissue after cerebral ischemia-reperfusion. The study was conducted on 28 male Wistar-albino rats. Control: No anesthesia or surgical procedure was applied. Sham: The carotid artery regions were opened and closed under general anesthesia. After the application, solvent application was performed for 1 week (1 ml DiOHF vehicle). Ischemia-Reperfusion: After isolating the carotid arteries, ischemia was performed by ligating them for 30 minutes, followed by reperfusion. Ischemia-Reperfusion + DiOHF: After ischemia was performed for 30 minutes, reperfusion was allowed. DiOHF supplementation was performed for 1 week. After one week of treatment, animals were killed and cerebellum tissues were taken to evaluate GRP78, HSP70, CHOP, Bcl-2 and Bax levels. While I/R increased GRP78 (p < 0,05), HSP70 (p < 0,05), CHOP (p < 0,05) and Bax (p < 0,05) values in the cerebellum, it resulted in significant downregulation of BCl-2 levels (p < 0,05). However, 3',4'-Dihydroxyflavonol application for 1 week corrected the deteriorations caused by I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R provides significant correction in endoplasmic reticulum stress related parameters caused by focal brain I/R in the cerebellum, suggesting that DiOHF may serve as a promising therapeutic candidate for defending cerebellar tissue from ER stress-related post-ischemic damage.

Background and objective: Women are twice as likely to have Alzheimer's disease (AD) than men and multiparity has been suggested to be a risk factor for dementia. The present study evaluated whether the lack of certain nutrients during pregnancy influences cognition while pregnant and in late adulthood using mouse model.

Methods: Non-targeted NMR analysis was conducted to assess changes in plasma nutrients and metabolites on gestation day 7.5 compared to day 1. Effects of choline intake during pregnancy on cognition and general health were evaluated in consecutive pregnancies. Mice were assigned to groups with normal diet, cholinesupplemented diet, or choline-deficient diet during pregnancy. Non-pregnant mice were included as controls. Behavioral analyses were performed during the second half of the first and fourth pregnancies, as well as at 12 and 15 months of age. The hippocampus was collected for RNA-seq analysis at 15 months of age.

Results and conclusion: Non-targeted NMR analysis revealed significantly lower levels of numerous plasma nutrients and metabolites including choline and its derivatives on gestation day 7 compared to day 1. Novel object recognition and Morris Water Maze tests revealed impaired cognition in pregnant mice compared to nonpregnant controls. Choline deprivation worsened the cognitive impairment during pregnancy and choline supplementation alleviated it. Furthermore, choline availability during pregnancy affected cognition and general health in late adulthood, with mice given a choline-deficient diet during pregnancy performed more poorly. RNA-Seq analysis indicates lasting effect of choline intake during pregnancy on hippocampal gene signatures in late adulthood. Choline deprivation was associated with more upregulation of proinflammatory genes, whereas choline supplementation showed upregulation of neuroprotective genes such as Prl, Gh, and hemoglobin (Hba and Hbb subunits). Together, the study shows that choline supplementation benefits cognitive health in women during pregnancy and in late adulthood.

Objective: Sleep problems are a common complaint among adults worldwide, however, the use of prescription and over-the-counter products may not always be an appropriate or desirable solution. L-theanine is a naturally occurring, non-protein amino acid that can be found in the leaves of the tea plant Camellia sinensis. Previous studies have reported that consumption of L-theanine can help to aid relaxation, without causing sedation or adversely impacting cognitive function. Building on these calming effects and results from recent pre-clinical studies, the aim of this review was to systematically appraise the scientific literature to establish whether dietary supplementation with L-theanine can also help to support sleep in humans.Methods: Electronic database searches of Ovid MEDLINE, PsycINFO, Embase, CENTRAL and Google Scholar were conducted from inception to 3rd February 2025. Retrieved articles were independently reviewed by three authors.Results: Thirteen eligible trials (n = 550) that examined the effect of L-theanine (50-900 mg/day) as a standalone intervention on sleep-related outcome measures were identified. This included two single-arm, open-label trials and eleven randomised controlled trials.Discussion: Based on the current evidence, supplementation with 200-450 mg/day of L-theanine appears to be a safe and effective way to support healthy sleep in adults. Among the included trials, beneficial effects were reported on both objective and participant-reported outcomes, including measures linked to sleep latency, maintenance and efficiency, perceived sleep satisfaction and feelings of refreshment and recovery on waking. Further high-quality trials using objective measures, into the mechanisms underlying these effects, and among those with clinical insomnia would provide further useful insights.