Nutritional Neuroscience最新文献

ABSTRACTObjectives: This research aimed to unravel the ameliorative potential of vanillic acid (VA) on lead acetate (LA)-induced cortico-hippocampal neurodegeneration in Wistar rats.

Methods: Forty (40) male Wistar rats (150-180 g) were randomized into four groups (A-D) (n = 10). LA and VA were freshly prepared daily for administration in dosages based on body weight (BW). Group A was administered normal saline as control; Group B received 200 mg/kg BW of LA; Group C 200 mg/kg BW of VA and 200 mg/kg BW of LA; Group D received 200 mg/kg BW of VA. The doses were selected based on existing protocols and sample size meeting the minimum estimate by power analysis. All administration was via a single daily oral dose for 45 consecutive days. Cognitive function tests including Y-maze and open field test were done. The rats were euthanized at the end of the treatment by cervical dislocation (n = 6, per group) and ketamine anesthesia + perfusion (n = 4 per group). The brains were dissected and processed for histological, biochemical, and immunohistochemistry studies.

Results: Our results revealed learning and memory deficits and neuropathological changes, such as decreased neuronal cell size and the disorganization of the neuronal network within the cortex and hippocampus of LA-induced rats, when compared to the control group. However, VA had protective function by attenuating neuronal degeneration, alleviation of cognitive deficit, and aided neuroprotection of pyramidal cells and astrocytes when compared to the LA-induced rats.

Discussion: VA shows protective effects against LA-induced neurodegeneration and cognitive impairment suggesting a therapeutic role in heavy metal neurotoxicity.

In recent years, obesity has reached pandemic levels and has been associated with a range of comorbidities, including anxiety disorders. Several studies have shown that the inclusion of legumes rich in dietary fiber can attenuate the adverse effects induced by high-fat diets. Jatobá-do-cerrado (Hymenaea stigonocarpa Mart.) stands out as a legume with high levels of dietary fiber and antioxidant compounds. The current study aimed to evaluate the effects of supplementation with Jatobá-do-cerrado flour on anxiety-like behavior and redox state parameters in rats on a high-fat diet. Male Wistar rats were divided for 126 days: Control- standard diet during 126 days; High-fat diet (HFD)- standard diet with added lard (20% w/w) for 126 days; Jatobá-do-cerrado flour (JCF)- standard diet with added Jatobá-do-cerrado flour (20% w/w) from 63^rd to 126^th day; Jatobá-do-cerrado flour + High-fat diet (JCF + HFD)- standard diet with Jatobá-do-cerrado flour (20% w/w) and lard (20% w/w) from 63^rd to 126^th. After the dietary treatments, the animals performed the Elevated Plus Maze, Light-Dark Box, and Open Field tests. The redox state of the adipose tissue and amygdala were analyzed. The HFD group showed anxiety-like responses in the tests, low antioxidant activity and high levels of lipid peroxidation in the adipose tissue and amygdala. Conversely, JCF + HFD group reduced anxiety-like behaviors and improved the antioxidant activity (adipose tissue and amygdala). In summary, the supplementation with Jatobá-do-cerrado flour improved antioxidant activity and also promoted an anxiolytic effect, suggesting its potential as a functional food and may be useful as an adjunct in the management of obesity and its related comorbidities.

Serotonin is a critical neurotransmitter that regulates a wide range of physiological, neurological, and behavioral functions. While peripheral serotonin, primarily produced in the gut, modulates gastrointestinal motility and vascular tone, central serotonin that is synthesized in the brain governs processes such as food intake, emotion regulation, memory, learning, and sexual behavior. Chronic consumption of a high-fat diet (HFD) disrupts serotonin signaling across the gut, brain, and the gut-brain axis, which supports bidirectional communication between these systems. Although the underlying mechanisms remain incompletely understood, this review explores how HFD alters serotonin signaling in both the gut and the brain. We report that HFD triggers pathway-specific changes that elevate serotonin levels in the gut while eliciting region-specific effects in the brain. HFD increases serotonin biosynthesis in the brain's raphe nuclei; however, enhanced 5-HT1A autoreceptor activity within these nuclei inhibits serotonin release to downstream projection areas. Coupled with increased serotonin degradation in these regions, this results in reduced serotonin levels in the hippocampus and hypothalamus. Additionally, our findings highlight a central role for microbial metabolites in mediating HFD-induced serotonergic dysfunction. Notably, short-chain fatty acids produced by gut microbiota, significantly contribute to the dysregulation of serotonin release and signaling under HFD conditions. Understanding these mechanisms may reveal new therapeutic strategies for managing serotonergic dysfunctions associated with gastrointestinal disorders, mood disturbances, and obesity-related complications.

Background: Morin hydrate is a polyphenolic flavonoid present in various vegetables, fruits, nuts, and sea products. It has been reported to offer multiple protective effects against a range of diseases, including cancer, cardiovascular, liver, neurological, metabolic, and renal disorders.Objective: This review highlights the molecular mechanisms and therapeutic potential of Morin in neurological diseases, including Parkinson's disease, Alzheimer's disease, traumatic brain injury, neuropathic pain, stroke, Huntington's disease, multiple sclerosis, amyotrophic lateral sclerosis, depression, anxiety, sleep, encephalopathy, schizophrenia, and psychosis, etc.Methods: The research and review articles were collected from the Pubmed, Scopus, Web of Science, and Google Scholar databases using 'Morin' and the above-mentioned neurological diseases as keywords.Results: The neuroprotective effects of Morin are primarily attributed to its ability to mitigate oxidative stress, inflammation, excitotoxicity, calcium dysregulation, mitochondrial dysfunction, neurotransmitter alterations, protein modifications, and enzymatic inhibition.Conclusion: Despite its promising pharmacological profile, the clinical adaptation of Morin for combating neurological diseases requires further validation through comprehensive preclinical and clinical investigations.

Background: Astaxanthin (AST) is a red pigment carotenoid with various pharmacological effects. It exerts powerful antioxidant and anti-inflammatory activities. However, there is still limited and sometimes contrasting data regarding the exact mechanism of AST in different inflammation models.

Objective: This study aimed to investigate whether AST attenuates oxidative stress and the inflammatory response in a mouse model of carrageenan (CAR)-induced inflammation and whether the wnt/β-catenin signaling pathway is involved in these potential protective effects.

Methods: Thirty-two male mice were randomly divided into four equal groups and pretreated with AST at 5 and 10 mg/kg doses for 14 days before CAR injection. The anti-inflammatory and anti-nociceptive effects of AST were assessed using the hot-plate test. Antioxidant enzyme activity and gene expression were evaluated by spectrophotometric analysis and qRT-PCR, respectively.

Results: Our findings demonstrated that AST produced neuroprotective effects, as evidenced by significantly reduced levels of malondialdehyde (MDA) and markedly increased levels of glutathione (GSH) and catalase (CAT) activity, as well as an increased latency of pain response on the hot plate. Furthermore, AST exhibited anti-inflammatory effects, as indicated by a significant reduction in the expression of glycogen synthase kinase 3β (gsk3β), tumor necrosis factor-alpha (tnf-α), and interleukin 6 (il-6) genes, alongside markedly increased expression of β-catenin and wnt genes in the brain.

Conclusion: In summary, our data indicate that AST pretreatment modulates CAR-induced oxidative stress and inflammation by promoting antioxidant enzyme activity, suppressing inflammatory cytokines, and activating the wnt/β-catenin signaling pathway.

Aim: This study aimed to evaluate the associations of adherence to the MIND and Mediterranean diets, as well as the dietary inflammatory index (DII), on the age of migraine onset and the disability among patients diagnosed with migraine with aura, migraine without aura, and chronic migraine.

Methods: This observational case-control study was conducted from 1 June to 30 September 2023, involving a total of 144 adult participants. The cohort included 84 newly diagnosed migraine patients, categorized as 45 without aura, 21 with aura, and 18 with chronic migraine, alongside a control group of 60 healthy individuals. Data were collected through a general information questionnaire, adherence scores to the MIND and Mediterranean diets, and the DII. Additionally, the patient group completed a migraine diagnosis form and the Migraine Disability Assessment Scale (MIDAS).

Results: Both in univariate and multivariable analyses, both low and moderate adherence are associated with increased odds compared to high adherence. In multivariable analyses, low adherence to the MIND diet increases the odds of migraines by 8.18 times (95% CI = 1.49-44.75), while moderate adherence increases them by 5.29 times (95% CI = 1.32-21.12). Low adherence to the MEDAS (OR =   9.90; 95% CI = 3.08-31.77) also shows a strong association with migraine in univariate analysis, but this association weakens in the multivariable analysis (OR = 3.14; 95% CI = 0.70-13.98). Higher quartiles (Q2-Q4) to DII were initially associated with migraines in univariate analysis but were not significant in multivariable analysis. Moreover, among the variables analyzed, chronic migraine shows a strong and significant association with MIDAS score compared to migraine without aura (β = 0.54, p < 0.001). However, MEDAS and DII do not meet the significance threshold for MIDAS. Only MIND is significantly associated with the age at migraine diagnosis (β = 0.38, p = 0.044).

Conclusion: The findings suggest that dietary patterns play a crucial protective role for patients with migraine. Nonetheless, further longitudinal studies with larger sample sizes are warranted to elucidate the relationship between dietary patterns, the onset of migraine, and the frequency and severity of migraine attacks.

Background: Evidence from randomised controlled trials demonstrates the modulatory effects of polyphenol consumption on the vascular system including improvements to cortical blood flow (CBF), microvascular blood flow, and large artery plasticity. Polyphenol-rich blackcurrants have been shown to inhibit monoamine oxidase, modulate brainwave spectral activity and modulate peripheral blood flow. This study assessed whether blackcurrant consumption can modulate blood flow in the shallow pre-frontal cortex, as measured using near infrared spectroscopy, during rest and under cognitive demand.

Methods: A randomised double blind, placebo-controlled balanced cross over design was used to assess the efficacy of a cold pressed blackcurrant juice drink (Blackadder cultivar, Neuroberry, Plant and Food Research Ltd.) standardised at 500 mg of total polyphenols upon attention and working memory and prefrontal cortical haemodynamics at rest and during cognitive load in 20 healthy young adults aged 18-35 years, following a 60-minute absorption period.

Results: Consumption of the Blackadder juice extract resulted in significant acute modulations of pre-frontal cortex haemodynamics during resting absorption and cognitive task performance as indicated by a decrease in deoxygenated haemoglobin [F(1,19) = 5.70, p = 0.027] and an increase in left hemisphere oxygenated haemoglobin during task performance [F(1.88,33.83) = 7.70, p = 0.002]. No effects on cognition were observed in this sample of healthy young adults.

Conclusion: Results from this trial outline the ability of a blackcurrant juice extract to increase cerebral blood flow during cognitive demand in healthy young adults. The effects of the juice extract in addition to other types of blackcurrant extracts upon acute and chronic brain function and blood flow deserve further investigation.Trial registration:ClinicalTrials.gov identifier: NCT01540123.

Objectives: Metabolic syndrome (MetS) is a global health issue linked to cardiovascular diseases, type 2 diabetes mellitus, and cognitive impairment. Chronic inflammation and oxidative stress associated with MetS condition contribute to cognitive decline, highlighting the need for therapeutic strategies to mitigate these complications. Vitamin D, a fat-soluble vitamin, plays a crucial role in physiological functions. Recent researches have highlighted the neuroprotective roles of vitamin D in several pathological conditions. Therefore, this review aims to summarize and discuss evidence from in vivo and clinical studies on the effects of vitamin D on brain pathologies and cognitive function in the context of MetS condition.

Methods: We searched articles published only in English, on PubMed Central from January 2000 to December 2023 using the following keywords: 1) "vitamin D", "metabolic syndrome", "brain"; 2) "vitamin D", "metabolic syndrome", "cognition"; 3) "vitamin D", "obesity", "cognition"; 4) "vitamin D", "obesity", "brain"; 5) "vitamin D", "hyperglycemia", "brain"; and 6) "vitamin D", "dyslipidemia", "brain", 7) "vitamin D", "T2DM", "brain"; and 8) "vitamin D", "T2DM", "cognition".

Results: Vitamin D treatment in animals with the MetS condition attenuated metabolic disturbances including inflammation, oxidation, hyperglycemia, obesity, and insulin resistance, and ameliorated cognitive dysfunction, suggesting the beneficial effects of vitamin D in the MetS condition.

Discussion: All the evidence indicates that vitamin D may be a potential therapeutic option to reduce cognitive dysfunction caused by metabolic syndrome.

Objectives: Obesity is a common public health problem, affecting 2.5 billion adults. Chronic high-fat diet (HFD) exposure, an experimental obesity model, strongly impacts the hypothalamic arcuate nucleus (ARC), a structure vulnerable to dietary-induced inflammation. Extra-virgin olive oil (EVOO) supplementation can be an interesting nutritional strategy to understand and/or treat obesity: EVOO has high nutritional quality, and acts on multiple molecular targets. We investigated EVOO supplementation's impact on metabolic parameters, satiety and hypothalamic inflammation in adult rats exposed to HFD from weaning, considering sex-specific outcomes.

Methods: 21-day-old Wistar rats were allocated into groups: (1) standard chow (SC); (2) SC+EVOO; (3) HFD; (4) HFD + EVOO. EVOO was administered daily by gavage. In adulthood, the behavioral satiety sequence was evaluated. Plasma leptin and ARC inflammatory markers levels were measured by ELISA technique. The immunofluorescence intensity of Toll-like receptor-4 (TLR-4) and ionized calcium-binding adaptor molecule-1 (IBA-1) were measured in the ARC.

Results: Chronic HFD-induced obesity was evidenced in both sexes, with increased body weight, body mass index, fasting blood glucose, caloric efficiency, and plasma leptin levels. EVOO supplementation prevented HFD-induced increase in weight gain and BMI in both sexes. HFD-fed animals had altered satiety. EVOO supplementation decreased immunoreactivity of IBA-1 in the ARC, also attenuates TLR-4 immunoreactivity, interleukin (IL)-6, IL-1β, and tumor necrosis factor-α levels in the ARC of obese animals.

Conclusion: Our results demonstrate that EVOO supplementation seemed promising, improving hypothalamic inflammation in obese animals, therefore might lead to the restoration of adverse metabolic consequences.

Context: Childhood obesity is a pervasive health issue, with sugar consumption implicated not only in its development but also in adverse effects on brain health. While extensive research has explored adult brain processes in response to sweet taste, there is limited understanding of how children's brains activate in similar, contexts.

Method: In this study, 34 children aged 8-12 undent food frequency and sweetness liking assessments before participating in a functional magnetic resonance imaging (fMRI) scan during a gustatory paradigm involving varying sweetness levels. Utilizing independent component analysis (ICA), we examined functional networks engaged during sweet taste perception and after swallowing.

Results: Our study identified distinct brain networks for tasting, swallowing, and a transitional stage linking the two. Children with lower BMI and higher sugar intake showed greater activation in the transition network, suggesting enhanced interoceptive sensitivity.

Conclusion: This novel investigation provides a foundational understanding of how sweetness exposure modulates brain networks in children responding to sucrose solutions, offering valuable insights into the interplay between sugar consumption, childhood obesity, and neural responses.