Nutritional Neuroscience最新文献

Compared with Panax ginseng (Asian ginseng), Panax quinquefolius (American ginseng) has received relatively little research attention. Nevertheless, across several clinical trials a common finding is that P. quinquefolius extracts improve aspects of mood, mental fatigue, and cognitive function. This review details the findings from double-blind, randomized, controlled clinical trials which included assessment of cognitive performance, fatigue, or mood, individually or in combination. Limited fatigue benefits were observed in cancer patients at high doses (2000mg). The most notable effects at lower doses (100mg-400 mg) included enhancement of attentional and working memory performance in healthy adults and in Schizophrenia patients. Several studies also highlighted potential mechanisms underlying the cognitive effects of P. quinquefolius. These include increased activation of frontoparietal neural circuits and, in the context of the gut-brain axis, alterations of the human gut microbiome composition. The effects are also consistent with cholinergic modulation. Such effects suggest that P. quinquefolius extract may have benefits to everyday cognitive function.

Background: Recent studies indicate that maintaining a healthy gut microbiota balance positively influences brain function through the microbiota-gut-brain (MGB) axis. Intestinal inflammation disrupts gut microbial homeostasis, exacerbates inflammatory and oxidative processes, and reduces beneficial microbial metabolites essential for brain health. These alterations may impair MGB axis signaling and increase intestinal and blood-brain barrier (BBB) permeability, facilitating the translocation of inflammatory mediators and potentially contributing to neurological dysfunction. Kefir has emerged as a fermented food with potential psychobiotic properties due to its ability to modulate gut microbiota and its metabolites. However, its effects on brain-related outcomes during intestinal inflammation remain poorly understood.Aim: To investigate the association between milk kefir consumption and selected brain biomarkers in IL-10^-/^- mice.Methods: Male C57BL/6 mice were allocated into four groups (n = 5/group): wild-type mice receiving water (WWT), wild-type mice receiving milk kefir (KWT), IL-10^-/^- mice receiving water (WKO), and IL-10^-/^- mice receiving milk kefir (KKO). Brain analyses included cytokine levels, antioxidant activity, tight junction protein expression, and short-chain fatty acids (SCFAs), while histological evaluation focused on the small intestine.Results: Kefir consumption was associated with improved intestinal morphology in IL-10^-/^- mice (p < 0.03), increased brain SCFA levels (p < 0.001), reduced malondialdehyde concentrations, and higher occludin expression in brain tissue.Conclusion: Overall, these findings suggest that milk kefir intake may influence specific brain biomarkers in IL-10^-/^- mice. These observations provide preliminary insights and support the need for further studies to elucidate the potential psychobiotic role of kefir in intestinal inflammation.

Neurodegenerative diseases (NDDs), including Alzheimer's, Parkinson's, Huntington's disease, and amyotrophic lateral sclerosis, are rising sharply across the globe. These incurable and progressive conditions lead to severe cognitive and motor impairments, diminish the quality of life, and place a substantial burden on healthcare systems. In response to this growing challenge, the present review offers an integrative and forward-thinking perspective focused on modifiable daily habits that have the potential to preserve brain health and reduce the risk of neurodegeneration. Mounting evidence reveals that everyday lifestyle choices, including food habits, physical activity, sleep, and stress, profoundly shape long-term cognitive outcomes. Neuroprotective diets such as the Mediterranean and ketogenic diets reduce oxidative stress, enhance mitochondrial efficiency, and promote neurogenesis, whereas the Western diet accelerates cognitive decline. Intermittent fasting and caloric restriction trigger autophagy and ketone production, offering metabolic resilience. Functional foods such as berries, walnuts, and leafy greens combat inflammation and oxidative damage. Physical activity and resistance training boost synaptic plasticity and neurotransmitter balance. In addition, high-quality sleep and effective stress control help preserve neuronal integrity and lower neuroinflammatory markers. By integrating insights from neuroscience, nutrition, and behavioral medicine, this review highlights how multiple modifiable factors, when adopted consistently, can work in synergy to preserve cognitive health, delay disease onset, and reduce progression.

Neurological disorders, including Alzheimer's and Parkinson's disease, are characterised by high morbidity and disability, representing a major global health challenge. A central obstacle in their treatment is the blood-brain barrier, a highly selective interface that limits drug delivery to the central nervous system. Rutin, a naturally occurring flavonoid, exhibits potent antioxidant, anti-inflammatory, and neuroprotective activities, yet its clinical utility remains constrained by poor solubility, low oral bioavailability, and restricted blood-brain barrier permeability. Recent advances in drug delivery and formulation science offer promising solutions. Nanoparticle encapsulation, peptide conjugation, intranasal delivery, and co-administration with absorption enhancers have been shown to improve rutin's solubility, metabolic stability, and central nervous system penetration in preclinical models. Mechanistic studies further reveal that rutin can modulate efflux transporters, regulate tight-junction proteins, and influence microglial activity and cellular metabolism, collectively contributing to enhanced neuroprotection. Experimental evidence highlights its potential to mitigate key neurodegenerative processes, particularly in Alzheimer's disease. This review synthesises current knowledge on rutin's pharmacological effects, limitations in bioavailability, and innovative strategies to improve blood-brain barrier penetration. By integrating mechanistic insights with advances in delivery technologies, this review underscores rutin's translational potential. Priority next steps include optimising delivery systems, establishing long-term safety, and conducting well-designed clinical trials to define efficacy and dosing.

Objectives: The microbiota-gut-brain axis highlights a significant diet, gut function, and mental health link. Although fermented foods benefit gut health, how their consumption patterns affect psychological well-being remains unclear. This study investigated associations between fermented food consumption patterns (variety, frequency and specific patterns), constipation, and psychological distress in adults.

Methods: This cross-sectional study included 400 adults (aged 18-65) in Turkey. A survey assessed socio-demographics (age, gender, BMI, education, and income) and fermented food frequency questionnaire. Psychological distress was measured using Depression, Anxiety, and Stress Scale-21. Gut function was evaluated using both Constipation Severity Instrument (CSI) and the Bristol Stool Scale for individual stool characterization. Data were analyzed using IBM SPSS 25.0. Associations were examined via correlation and multiple regression analyses (covariates-adjusted). The indirect effect of consumption patterns on distress through CSI was tested using PROCESS Macro (v4.3, Model 4) with 5000 bootstrap samples.

Results: Contrary to expectations, a greater fermented food variety was associated with poorer psychological well-being. Pattern analysis revealed that the 'Low Variety + Medium-High Frequency' pattern was associated with the best psychological state. Conversely, a 'Medium-High Variety + Low Frequency' pattern predicted significantly worse psychological outcomes. This negative effect was fully mediated by increased constipation severity (p < 0.05).

Conclusions: The fermented food-psychological health relationship is pattern-dependent. Consistent consumption of a limited variety was more strongly associated with positive gut-brain axis-related outcomes than sporadic consumption of a wide variety. These results emphasize incorporating specific, sustained fermented food patterns into dietary recommendations and warrant longitudinal and interventional studies.

Background: The gut-brain axis is well known to have a bilateral relationship. Recent research has shown the positive influence of probiotic supplementation on mental flexibility and stress scores among healthy elderly population. However, no similar research has been conducted for young children.

Aim: To investigate the influence of probiotic supplementation on the developmental progress of healthy children.

Methods: A prospective, randomised, double-blind, placebo-controlled trial was conducted among 105 healthy children, who received either probiotic or placebo supplementation over a six-month period. Of those, 51 were allocated to the probiotic group and 54 to the placebo group. Pre - and post-developmental assessments were conducted using the ASQ-3 and ASQ:SE-2 questionnaires.

Results: Per-protocol analysis showed that children in both the probiotic and placebo groups demonstrated significant improvements in 3 of the 6 ASQ-3 developmental domains. However, baseline analysis by age group revealed significant differences in 3 of the 6 ASQ-3 domains, with children older than 44 months showing better developmental scores. Moreover, increasing age and higher consumption of fruits and vegetables were identified as significant confounders associated with developmental progress.

Conclusion: This first-of-its-kind study conducted among healthy preschoolers concludes that probiotic supplementation did not significantly influence developmental progress. However, the study was underpowered for its primary outcome. Future large-scale studies involving diverse populations are recommended.Trial registration: Australian New Zealand Clinical Trials Registry identifier: ACTRN12622000153718..

Objective: Docosahexaenoic acid (DHA) is indispensable for neurological health, yet its therapeutic potential is hampered by poor bioavailability and non-specific brain distribution. We hypothesized that co-administering DHA with specific molecular carriers - eicosapentaenoic acid (EPA) or phosphatidylserine (PS) - would exploit distinct cellular transport pathways to achieve region-specific brain enrichment and associated neuroprotection.

Methods: By dietary intervention using C57BL/6J mice, we employed regional lipidomics, ELISA, and western blotting to assess brain fatty acid incorporation, neurotrophic factor levels, inflammatory signaling, and transporter expression following supplementation with DHA alone or in combination with EPA or PS.

Results: Lipidomic analyses revealed striking, carrier-dependent spatial modulation of DHA. Co-administration with EPA enriched the cortex and striatum, while PS co-administration preferentially targeted the hippocampus and cortex. Mechanistically, both carrier-DHA complexes enhanced the expression of the key blood-brain barrier (BBB) transporter MFSD2A. Functionally, this precision delivery activated distinct neuroprotective programs. PS + DHA robustly upregulated the CREB-BDNF neurotrophic pathway, while EPA + DHA uniquely suppressed the NF-κB pathway, demonstrating potent anti-inflammatory effects. These results demonstrate that the choice of molecular carrier dictates both the spatial distribution of DHA and the nature of the ensuing neuroprotective response.

Discussion: Our findings establish that dietary co-supplementation with specific lipid carriers enables precise spatial delivery of DHA by engaging specific transporters, thereby activating distinct neuroprotective programs in a region-specific manner. This work provides a mechanistic framework for a precision nutrition strategy, tailoring DHA formulations to target specific neuroanatomical and cellular vulnerabilities in neurological disorders.

Introduction: By 2050, the global population aged 60+ is expected to reach two billion. As the population ages, the prevalence of neurodegenerative disorders will increase, while depression and anxiety will continue to be major causes of disability. A diet rich in antioxidants can positively impact cognitive function and protect against psychological disorders.

Objective: to summarize the evidence of the impact of the MIND diet in reducing risks or slowing neurodegenerative and psychological diseases.

Methodology: The data were collected by searching electronic databases, including PubMed and Science Direct, until September 2023. The search terms included 'Alzheimer's, Anxiety, Brain Health, Cognitive Decline, Dementia, Depression, Parkinson's, MIND diet, and psychological disorders.' Peer-reviewed studies conducted on individuals aged 18 or older were included. 135 papers were identified and reviewed. 26 full-text, relevant original articles were included.

Results: The study analyzed a sample of 37 to 16,058 participants, ages 20-97. Among the identified studies, 6 RCTs, 11 cross-sectional studies, and 9 longitudinal studies were analyzed. The results indicate that adherence to the MIND diet slows cognitive decline and positively influences cognitive function and verbal memory in later life, reducing the risk of developing Parkinsonism, non-motor symptoms, depressive symptoms, and lowering stress levels.

Conclusion: Our systematic review implies that the MIND diet can enhance cognitive health and is highly beneficial for mitigating risks of dementia, physiological diseases, anxiety, and depression due to its superior antioxidant and anti-inflammatory activities. However, further research is required to evaluate its long-term effects on health.

Nutrition is crucial for mental well-being and enhancing cognitive performance. Food restriction (FR), a moderate reduction in food intake, results in multiple effects on brain function. Most studies of FR have been conducted on adult animals rather than young ones. This study examines the acute effect of early-onset FR, starting at four-week age, on behavioral performance, molecular changes, and histological changes. Young mice were randomly assigned to four experimental groups: Control-1, Control-2, FR1, and FR2 groups. The control groups had free access to food, while the FR1 and FR2 groups experienced food deprivation for 12 h each day (7 pm to 7 am) over periods of 30 and 60 days, respectively. The average body weight of the mice was measured at the start and end of the study. The exploratory action, anxiety-like behaviors, and passive avoidance memory were evaluated using open field, elevated plus maze, and shuttle box devices. Histologic changes were assessed using H&E staining. The antioxidant capacity and alterations in gene expressions (BDNF and Inflammatory markers) were estimated in the hippocampus using FRAP methods and qRT-PCR, respectively. In young mice, 12-hour daily restricted feeding negatively affects cognitive, psychological, and exploratory behaviors. FR leads to a drop in antioxidant capacity, histological changes in the CA1 and CA3 regions, increased expression of inflammatory genes, and reduced BDNF expression. In summary, our outcome indicates that FR worsens brain oxidative stress, promotes inflammation in the brain, and eventually damages hippocampal neurons in young mice.

Autism Spectrum Disorder (ASD) has been linked to metabolic disturbances in prior research. This pilot study explored plasma and urinary amino acid profiles in a cohort of Jordanian boys with ASD (n = 17) and their mothers, comparing them to neurotypical controls (n = 17). Amino acid concentrations were quantified using Amino Acid Analyzer system, which integrates: High-performance liquid chromatography (HPLC); cation exchange chromatography for separation; and post-column ninhydrin derivatization, l. Our analysis revealed preliminary correlations, including a significant association between urinary arginine levels in children with ASD and their mothers (r = 0.52, p = 0.031). Furthermore, distinct amino acid patterns were observed across ASD severity levels. When evaluating individual amino acids as biomarkers, several showed fair diagnostic accuracy (AUC 0.7-0.8) in internally cross-validated ROC analyses. The observed patterns suggest a complex interplay of genetic factors e.g. Potential inheritance of metabolic enzyme variants, environmental influences (e.g. Shared dietary habits or toxin exposures, and physiological adaptations). These findings suggest that amino acid dysregulation may be involved in ASD and warrant further investigation. However, the small sample size necessitates caution, and these results should be validated in larger, more diverse cohorts to assess their generalizability and potential clinical relevance.