Nutritional Neuroscience最新文献

Objective: Autophagy is a critical cellular mechanism that ensures the breakdown of damaged or unnecessary components. This process helps ensure cellular health by maintaining cellular balance, protecting cells from stress, and providing an alternative energy source during metabolic stress. Disruptions in autophagy have been linked to neurological disorders.Method: In this review, the neuroprotective effects of Kaempferol through autophagy modulation are elaborated. Methods: An electronic search in scientific databases was performed to find relevant studies exploring the neuroprotective effects of kaempferol mediated via modulation of autophagy.Results: Kaempferol, a natural flavonoid found in fruits, vegetables, and plant-based products like tea, has been shown to demonstrate a variety of health-promoting properties, including antimicrobial, antioxidant, and antiinflammatory effects. This review summarizes the current understanding of how Kaempferol modulates autophagy and discusses its potential impact on various neurological disorders, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, ischemic stroke, and depression. Studies increasingly indicate that Kaempferol could be a vital factor in maintaining neural health by influencing autophagy mechanisms.Conclusion: Numerous studies have established Kaempferol's neuroprotective potential through autophagy regulation, which suggests opprotunities for potential therapeutic applications.

Objectives: Patients with Ulcerative Colitis (UC) are susceptible to emotional disturbance, which could negatively affect the condition itself. Meanwhile, certain probiotics have been proven to alleviate emotional disturbance, and improve disease status in UC. Yet little is known about probiotic's efficacy on UC patients with emotional disturbance.

Methods: Sixty patients were recruited, diagnosed as having mild to moderate UC and with anxiety and/or depression disorders. Participants were then randomly assigned to a control group receiving conventional treatment (mesalazine ≤4 g) or a probiotic group receiving probiotic LAB combined with conventional treatment for 8 weeks. At the commencement and conclusion of the study, questionnaires were administered to determine patients' improvements in emotional disturbance and disease activity. Stool samples were collected concurrently to estimate alterations in fecal microbiota.

Results: At 8 weeks, 65.4% of patients in the probiotic group had relieved anxiety disorder, compared to 34.6% in the control group (p = 0.03). Improvement on depression was higher in the probiotic group (53.8%) than the control group (30.8%), though without significant differences (p = 0.09). Both groups had reduced Modified Mayo Scores (MMS). Mayo Endoscopic Sub-score (MES) dropped significantly in the probiotic group (p = 0.02) but not in the control group. Fecal samples sequenced by 16S rRNA showed a significant increase in Firmicutes after receiving probiotics, and no significant differences were detected in the control group.

Discussion: This randomized trial demonstrated that supplementation with probiotic LAB could restore the abundance of Firmicutes, improve anxiety disorder, and reduce MES in UC patients with emotional disturbance.Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT04006977, date October 2019.

Background: Vascular cognitive impairment (VCI) is the second most common cause of dementia. Chronic cerebral hypoperfusion (CCH) is the major driving factor for vascular pathology and clinical manifestations of VCI, leading to amino acids (AA) metabolic abnormalities, including glutamate (Glu), gamma aminobutyric acid (GABA), and branched chain amino acids (BCAAs). There is a positive association between BCAAs and cognitive function. However, the specific mechanism is unclear. In this study, we investigated the possible mechanisms underlying the beneficial effects of exogenous BCAAs on VCI.

Methods: All rats, except for the Sham group, underwent bilateral carotid artery ligation surgery (2-vessel occlusion, 2VO) and were randomly divided into 5 groups: Sham, 2VO, 2VO + 2.5% BCAAs, 2VO + 5% BCAAs, 2VO + 10% BCAAs. The sham and 2VO groups were fed a standard diet, while the others received BCAA-supplemented diets. After 4 weeks, we measured cognitive function, the content of AA and expression of related proteins, as well as synaptic related structures and functions.

Results: We found that 2VO led to cognitive impairment, a decrease in BCAA and GABA contents, and an abnormal increase in Glu content. Additionally, the expression levels of AA-related proteins (BCAT1, GDH, GAD,VGLUT1, EAAT2), and synapse related proteins (PSD95, synapsin I, p-CAMK II α) were found to be decreased and synaptic structure was disrupted in 2VO rats, which were reversed after BCAA diets.

Conclusions: This study suggested that supplementation with exogenous BCAAs can improve CCH-induced VCI by regulating glutamate metabolism and transport, while also improving synaptic structure and function.

Gut-brain axis has emerged as a promising strategy for managing depression. Probiotic supplements, which modulate the gut microbiome, are suggested to enhance gut-brain communication and improve depressive symptoms and cognitive function. However, the acceptance of probiotics in managing depression remains contentious. This study aimed to evaluate the effects of probiotics on depression through meta-analysis and to assess their mechanisms of action, focusing on changes in gut microbial composition and neural mechanisms. A total of 12 randomized controlled trials from PubMed, Web of Science, and Scopus, up to January 1, 2024, were included. Nine studies consistently demonstrated improvements in depressive symptoms, gut microbiota, inflammatory markers, cognitive function, and mood regulation. The meta-analysis indicated a significant reduction in depressive symptoms with probiotics compared to placebo, with a mean difference of - 1.94 (95% CI = -3.56 to - 0.32, p = 0.02, I₂ = 69%). The Hamilton Depression Rating Scale (HAM-D), which showed substantial improvement, with a mean difference of - 3.27 (95% CI = -6.42 to - 0.12, p = 0.04, I₂ = 82%), is a preferred tool for further studies due to its comprehensive symptom coverage and strong psychometric properties. Probiotic strains such as Lactobacillus plantarum subspecies JYLP-326 and Bifidobacterium breve CCFM1025 were particularly effective, while multi-strain probiotics generally showed more consistent effects than single-strain interventions. Probiotics show promising potential in alleviating depression through their anti-inflammatory effects, gut microbiota modulation, cognitive function enhancement, and possible influence on brain structure and neurotransmitter systems. Despite some variability in trial results, this review provides updated insights for medical practitioners, highlighting probiotics as a viable treatment option for depression.

Background: Stroke is a leading cause of disability and burden worldwide. Recent studies have highlighted the link between undernutrition and the risk of hemorrhagic transformation in ischemic stroke, indicating that undernutrition may directly affect stroke severity. However, the extent to which nutritional status at stroke onset influences stroke severity remains unclear.

Aims: This study aimed to investigate the relationship between undernutrition on admission and stroke severity in patients with acute stroke.

Methods: This retrospective cross-sectional study included hospitalised patients with acute stroke. Nutritional status was determined using the Global Leadership Initiative on Malnutrition (GLIM) criteria. Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS). Multiple linear regression analyses identified covariates associated with NIHSS scores, including GLIM-defined undernutrition and risk of undernutrition according to the Mini Nutritional Assessment Short Form and the Geriatric Nutritional Risk Index.

Results: This study included 563 patients with acute stroke (median age, 81 years). Those with GLIM-defined undernutrition had high NIHSS scores. Multiple regression analysis revealed that GLIM-defined undernutrition (β = 0.136, p = 0.002), risk of undernutrition according to the Mini Nutritional Assessment Short Form (β = 0.160, p < 0.001), and risk of undernutrition according to the Geriatric Nutritional Risk Index (β = 0.081, p = 0.043) were independently associated with increased NIHSS scores.

Conclusion: The presence or risk of undernutrition at the time of hospital admission is associated with severe stroke in patients with acute stroke. This finding indicates the necessity for further research to understand the impact of nutrition on stroke severity and develop effective prevention strategies.

Introduction: Puberty is a crucial developmental phase influenced by neuroendocrine signals involving various neuropeptides and hormones. The impact of various diet combinations on the initiation of puberty in female rats was studied, along with the crosstalk between hypothalamic neuropeptides that might influence it.

Methods: Weaned female Wistar rats were segregated into five groups and given different diets for a duration of 21 d. The diet included high-fat, high-carbohydrate, high-protein, cafeteria diet and standard chow. Throughout the 21-day period, body weight, vaginal opening and blood samples were recorded. Post sacrifice parameters like hormonal analysis, gene expression, protein expression and Immunolocalization were performed.

Results: The High Fat Diet (HFD), High carbohydrate Diet (HCD), and Cafeteria diet (CafD) groups exhibited early vaginal opening, increased body weight, elevated somatic indices, and Follicle-stimulating Hormone (FSH), Luteinizing Hormone (LH), and estradiol levels were elevated in regards to the control group. Gene expression analysis showed upregulation of Kiss1, Kiss1r, Pomc, Lep, Lepr, and Gnrh, while Npy, Agrp, and Mkrn3 were downregulated. Protein expression studies confirmed the increased levels of KISS1, KISS1R, LEPR, and POMC, particularly in the HFD and HCD groups. Histone acetylation analysis revealed higher global acetylation in the hypothalamus of HFD and HCD groups.

Discussion: This study highlights the significant role of dietary composition in modulating pubertal onset through the neuroendocrine pathways. These findings suggest that high-fat and high-carbohydrate diets expedite puberty by altering the expression of key hypothalamic neuropeptides and hormones. This underscores the importance of nutrition in reproductive development and its broad implications for adolescent health.

Objective: Alzheimer's disease (AD) is the most prominent neurodegenerative disease in the world, with complex and multifaceted pathologies. Current symptomatic medications merely attenuate symptoms of the disease with substantial side effects, neither slowing down nor preventing the disease's progression. Despite the increasing number of studies drawing a prominent role of epigenetic modulations in this disease, however, little is known about the role of nutrients in affecting epigenetics in AD.Methods: This review synthesised current knowledge of epigenetic alterations, such as DNA methylation, histone modifications, and non-coding RNAs, based on the findings from AD-related in vitro, in vivo, and clinical studies, and explores the relationship between nutrient exposure and their epigenetic effects in AD.Results: Evidence indicates that epigenetic mechanisms play a significant role in ageing and the development of AD. An expanding body of research suggests that nutrients can modulate epigenetic processes in AD, with potential benefits, including the regulation of amyloid-beta and tau pathology, reduction in oxidative stress, and improvement in cognitive function. However, the precise mechanisms of action (MOA) remain unclear, largely due to inconsistent and contradictory findings across the literature.Conclusion: This review highlights the influence of nutrients on epigenetic modulations in AD, underscoring the need for more comprehensive analyses of the underlying mechanisms. Future studies, involving larger and more diverse populations, are warranted to establish a clearer relationship between nutrient exposure and epigenetic changes in AD. Such insights may pave the way for developing nutrient-based epigenetic interventions as potential therapeutic strategies in AD.

Background: Activities of daily living (ADL) disability and dementia are major contributors to the growing burden of ageing-related public health challenges in China.

Objective: To evaluate the independent and combined associations of vitamin D deficiency and dyslipidemia, particularly low high-density lipoprotein cholesterol (HDL-C), with ADL disability, dementia, and their composite outcome among Chinese older adults.

Methods: We analyzed data from 2107 community-dwelling Chinese adults aged ≥65 years participating in the 2014 wave of the Chinese Longitudinal Healthy Longevity Survey (CLHLS). Multivariable logistic regression models were used to estimate adjusted odds ratios (ORs) and 95% confidence intervals (CIs).

Results: Vitamin D deficiency (<20 ng/mL) was independently associated with higher odds of the composite outcome, ADL disability, and dementia. Low HDL-C (<1.0 mmol/L) was significantly associated with the composite outcome and ADL disability, but inversely associated with dementia. Notably, participants with both vitamin D deficiency and low HDL-C had dramatically elevated risks: OR = 8.27 (95% CI: 3.98-17.20) for the composite outcome and OR = 7.78 (95% CI: 3.74-16.17) for ADL disability. A significant multiplicative interaction between vitamin D and HDL-C was observed for the composite outcome and ADL disability (both P-interaction < 0.001), but not for dementia (P-interaction = 0.591).

Conclusions: Vitamin D deficiency and low HDL-C levels are independently and synergistically associated with increased risk of functional and cognitive impairment in Chinese older adults.

Objectives: High-fat diet is well-known to contribute to systemic and central nervous system dysfunction and represents a modifiable risk factor for cognitive decline. A recent surge of new weight loss medications has demonstrated that caloric restriction by reduced overeating has been successful at mitigating peripheral markers of inflammation and metabolic dysfunction. However, less is known regarding such effects of dietary reversal within the brain.

Methods: Male mice received high-fat diet (HFD; 60%kCal fat) from 6 weeks of age (JAX #380050). At 14 weeks, half of the mice were reversed (Rev = 9) to a standard diet (14%kCal fat) while the other half (HFD = 10) remained on HFD for an additional 2 months. Weight, frailty, peripheral cytokines, and behavior were recorded at baseline and again at 1 and 2 months after dietary reversal. Mice were sacrificed at 22 weeks of age and terminal measures of brain neuroinflammation and metabolism were evaluated.

Results: In contrast to mice on continuous HFD, the mice in the Rev group lost weight, had lower frailty scores, preserved spatial discrimination, altered peripheral cytokine profiles, lower hippocampal GFAP, increased hippocampal MCP1 and IL4, improved hippocampal and midbrain insulin tone, and differentially altered TRIB3 in the hippocampus and midbrain.

Discussion: Early dietary reversal was effective at preventing the inflammatory, metabolic, and cognitive effects of sustained HFD with divergent effects on metabolic markers (TRIB3) depending on brain region.

Background: Recent research highlights the central role of emotion in psychopathology, with Panksepp's Affective Neuroscience Theory identifying seven primary emotional systems critical for mammalian survival. Although this framework has advanced understanding of disorders such as depression and addiction, its application to eating pathology remains limited.

Objective: The present study integrates affective neuroscience with behavioural analysis, conceptualizing emotions not merely as neural activations but as classes of behaviour shaped by phylogenetic selection and ontogenetic contingencies.

Methods: Eating disorders, characterized by maladaptive eating patterns that impair physical and psychological functioning, are examined here as emotional-behavioural phenomena maintained by reinforcement processes. This cross-sectional, correlational study investigated associations between emotional systems and disordered eating.

Results: Weak but statistically significant correlations were found between negative emotional systems (FEAR, PANIC/GRIEF, RAGE) and disordered eating (r ≈ .15-.25, 95% CI [.07, .35]), suggesting that difficulties in emotion regulation may act as antecedents and reinforcers of maladaptive coping behaviours. Positive emotional systems (PLAY, CARE, SEEKING) showed no significant relationships, indicating heterogeneous reward contingencies among individuals with eating pathology. Exploratory gender-stratified analyses revealed small differences in emotional correlates but no moderation effects, underscoring similar functional mechanisms across sexes.

Conclusions: Findings are interpreted within a functional-analytic framework, proposing that disordered eating is maintained by negative reinforcement, reducing aversive private events such as shame, fear, or panic. Clinically, results highlight the need for integrated, context-sensitive interventions that target emotion regulation and avoidance mechanisms across genders.