Nutritional Neuroscience最新文献

Objective: To investigate the impact of drinking different caloric sweeteners from immaturity to young adulthood on hypothalamic controlled physiological functions and hypothalamic global gene expression using a rat model.

Methods: Young female Sprague-Dawley rats (age 28 days) were randomly assigned (n = 7 rats/group) to drink water sweetened with 13% (w/w) sugar as either high fructose corn syrup (HFCS), sucrose, fructose, or water (control) for 8 weeks. Hypothalamic controlled physiological function measurements included: energy intake, stress, and estrous cycles. RNA-sequencing (RNA-Seq) was used to investigate global differentially expressed genes (DEGs) in the hypothalamus.

Results: Rats drinking HFCS and sucrose solution increased liquid intake, but reduced food intake. Rats drinking HFCS had the highest (p < 0.05) absolute adrenal weight, which is indicative of chronic stress, and had lengthened estrous cycles. The DEGs with the highest fold changes in the hypothalamus of rats drinking HFCS compared to sucrose and fructose were involved in circadian sleep cycles, neuronal processes, and Engrailed-2 (En2) identified in autism spectrum disorder (ASD).

Conclusion: Among the different caloric-sweetened solutions, young female rats drinking HFCS solution showed food selectivity, elevated basal stress, and reproductive irregularity, which are characteristics associated with ASD. RNA-Seq revealed DEGs in rats drinking HFCS solution, included disrupted circadian sleep cycles, neurotoxicity, and ASD. The results of this preclinical study suggest that HFCS intake should be limited due to its potential for increasing the risk of neurodevelopmental disorders.

Objectives: Chronic microglial activation drives neuroinflammation, contributing to neurodegenerative diseases and cognitive decline. Walnuts and blueberries (BB) have been demonstrated to reduce neuroinflammation, but it is unknown whether they act synergistically to enhance the effects seen with individual treatment. This study examined the individual and synergistic effects of walnut oil (WO) and BB on lipopolysaccharide (LPS)-induced neuroinflammation in rat microglial cells. The effects of pretreatment duration and concentration were also explored.

Methods: Rat microglial cells were pretreated for 48 hours, one, two, or four weeks with 0.05, 0.1, 0.2, 0.5 and 1.0 mg/mL BB extract, WO or WOBB, followed by exposure to LPS (100 ng/mL). Cell viability was assessed and standard immunochemical techniques were used to measure levels of the inflammatory biomarkers: nitrite, inducible nitrous oxide synthase (iNOS), and cyclooxygenase-2 (COX-2).

Results: BB, WO, and WOBB reduced LPS-induced nitrite, COX-2 and iNOS relative to control, with higher concentrations and longer treatment durations typically being most beneficial. All treatments showed similar ability to reduce iNOS expression, while BB had a stronger effect on reducing nitrite production than WO and WOBB. There were no significant differences between treatment effects on COX-2 expression.

Conclusion: BB and WO each reduced LPS-induced inflammation in microglia, but their combination was not more effective, suggesting no synergistic effect. This result suggests that they may work through similar mechanisms to attenuate inflammation in microglia. Overall, the reduction in neuroinflammation shows that the addition of BBs or walnuts to the diet may attenuate neuroinflammation linked to neurodegeneration.

Background: Alzheimer's disease (AD) and Multiple sclerosis (MS) are progressive neurodegenerative conditions. AD is characterized by neuroinflammation, plaques, tangles, and synaptic loss, while MS involves inflammatory demyelination. Although AD and MS have different pathogenesis, they may share some neurodegenerative mechanisms, so similar therapeutic strategies could potentially be effective for both. Research suggests that natural substances such as carotenoids may be beneficial for neurological disorders. Notably, Astaxanthin (AXT) has demonstrated promising effects as an adjunct therapy.

Methods: In this review, we aimed to shed light on the effects of AXT on MS and AD by searching published articles from inception to 1 August 2024, in the Scopus, Google Scholar, PubMed, and PubMed/Medline databases.

Results: The therapeutic effects of AXT in neurodegenerative disorders are associated with its antioxidant, anti-inflammatory, anti-apoptotic, and neuroplasticity improvement properties. Literature have confirmed that AXT can positively impact AD by modulating anti-inflammatory and pro-inflammatory cytokines, mitochondrial function, amyloid beta production, and microglial activation, which collectively leads to memory and learning enhancement. Additionally, AXT has demonstrated advantages in MS by reducing demyelination and preserving nerve functions through its effects on pro- and anti-inflammatory cytokines, as well as promoting the differentiation of oligodendrocyte precursors into mature oligodendrocytes.

Conclusion: AXT, as a promising versatile adjunctive neuroprotective therapy, can influence multiple recovery pathways rather than focusing on a single target or mechanism. According to the results of preclinical studies, we can recommend assessing AXT effects in clinical trials of AD and MS.

Objective: Comparison of the effect of acute daytime fasting on mood, satiety, and neurotrophic factors in females with (OB) and without obesity (N-OB).

Methods: Non-randomized single-arm feasibility trial. Data were collected at an outpatient clinic and from real-world settings. Participants were evaluated after 10 h of nocturnal fasting (T1) and following a 10-hour diurnal fasting period (T2) after consuming a standardized breakfast. Mood, subjective feelings of satiety, food cravings, and neurotrophic factors brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and glial cell line-derived neurotrophic factor (GDNF) were assessed.

Results: Fifty-four participants were enrolled in the study [mean age 31 (SD 9)]. One participant from the OB group dropped out before T2, leaving 53 participants (N-OB: n = 29, OB: n = 24). Both groups experienced increased hunger and decreased satiety and fullness after T2. Females with obesity had a greater increase in hunger (p = 0.02). Depression and anger symptoms increased in the OB group, whereas fatigue increased in the N-OB group after T2. NGF increased slightly in the N-OB group after T2, while BDNF and GDNF remained unchanged.

Conclusion: Daytime fasting during daily activities affects mood and eating behavior, especially in females with obesity. Fasting interventions should be tailored to individual needs, considering these differential effects.

Trial registration: ClinicalTrials.gov identifier: NCT03532672.

Objective: To identify dietary total antioxidant capacity (DTAC) in people with MS (PwMS) and evaluate its interrelation with nutritional status and disease progression.

Methods: Cross-sectional, quantitative study with 127 patients with MS recruited from the Interdisciplinary Center for Assistance, Research and Teaching in Neuroimmunology (CIAPEN) (Fortaleza, Ceará, Brazil). The clinical parameters were clinical phenotype, the expanded disability status scale (EDSS), the medical research council (MRC) muscle scale, and Magnetic Resonance Imaging (MRI) evaluation. Weight and height measurements were obtained to calculate the body mass index (BMI), waist circumference (WC) and estimate body fat percentage (BF%). The DTAC was estimated using food intake data from the 24DR and the intake of antioxidant supplements.

Results: As for the nutritional status, it was found that 48 (37.80%) and 64 (50.39%) had excess adiposity according to the BMI and BF%, respectively, and 67 (53.60%) had elevated WC. Higher DTAC was associated with higher WC (r = 0.192, p = 0.032) and BF% (r = 0.246, p = 0.005); and higher intake of energy (r = 0.418, p < 0.001). There was no association between the clinical phenotype of the disease, the EDSS, the presence of visible lesions and the DTAC tertiles. However, in the unadjusted model, it was observed that the second tertile of DTAC reduced by 64% (OR = 0.36; 95% CI: 0.14-0.96) the individual's chance of having lower muscle strength, assessed by the MRC muscle scale.

Conclusion: Healthy nutrition, especially sufficient intake of dietary antioxidants, should be encouraged in PwMS.

Background and objectives: Stress in day-to-day life affects the body system differently by altering homeostasis and biological processes. The foremost sign of chronic stress-induced disorders is reflected in behavioral activity. Chronic stress affects the brain negatively, it modulates neurobehavioral activity and impairs the associated activities like learning, memory, and cognition. Emerging evidence suggests that virgin coconut oil (VCO), is an abundant source of natural antioxidants with anti-inflammatory, antidepressant, and neuroprotective potential. However, VCO's efficacy in ameliorating chronic restraint stress-induced abnormal changes is rarely understood. Hence, we aimed to evaluate VCO's neuroprotective potential in attenuating chronic restraint stress-induced neurobehavioral and biochemical alteration in rats.

Methods: A total of eighteen male Wistar rats were allocated into three groups (n = 6/group): Control (C) - saline (5 ml/kg/21 days), Stress (S) - restraint stress (6hrs/day/21 days), and Test (S + VCO) (6 hrs/day+5 ml/kg VCO for 21 days). The behavioral (Radial arm maze (RAM)) and biochemical (corticosterone (CORT)), reduced glutathione (GSH), and malonaldehyde (MDA) parameters were analyzed to determine the neuroprotective effect of VCO.

Results: The VCO-treated group has shown a significant increase in the percentage of correct choice entries and a reduction in error entries, highlighting an improvement in working and reference memory. Moreover, there was a substantial elevation in GSH, and a reduction in MDA and CORT levels, indicating a potent antioxidant activity of VCO. Additionally, significant body weight gain and reduced adrenal gland weight were noted in VCO-treated rats.

Conclusions: Our findings signify that VCO has therapeutic potential to improve spatial learning memory and antioxidant status in chronic restraint stress rats.Schematic depiction of the protective effect of virgin coconut oil on chronic restraint stress rats.

HighlightsVCO exhibits notable neuroprotection and convalesces the neuron.VCO reduces lipid peroxidation in the brain of chronic restraint stress rats.VCO retrieves spatial learning and memory in chronic restraint stress rats.Oral administration of VCO in rats prevents oxidative stress damage in the brain.

Background: Lectins are carbohydrate-binding proteins found in plants and animals. While they serve essential biological functions, certain plant-derived lectins-especially from legumes-may exert neurotoxic effects through the gut-brain axis. The growing intake of raw plant-based foods, including lectin-rich sprouts, raises safety concerns.Objective: To evaluate the neurotoxic potential of a galactose-specific lectin (BS-Gal) isolated from bean sprouts, with a focus on oxidative stress, energy metabolism, and neuroinflammation in mice.Methods: Mice were chronically administered BS-Gal orally. Brain regions (substantia nigra, cerebellum, brainstem) were analyzed for oxidative markers, metabolic enzymes, apoptotic signals, and inflammatory mediators using biochemical assays and immunoblotting.Results: BS-Gal significantly increased hydrogen peroxide, nitric oxide, and malondialdehyde levels, alongside reduced antioxidant enzyme activities, indicating oxidative damage. Glycolytic and citric acid cycle enzymes were suppressed, suggesting disrupted cellular metabolism. Apoptotic analysis revealed elevated pro-apoptotic markers (Bad, Bax) and reduced anti-apoptotic proteins (Bcl-2, Bcl-xL). Neuroinflammation was evident via NF-κB activation, increased proinflammatory cytokines (TNF-α, IL-6, IL-1β), and decreased anti-inflammatory markers (IκB-α, IL-4, IL-10, TGF-β).Conclusion: Chronic oral exposure to BS-Gal induces oxidative stress, metabolic dysfunction, and neuroinflammation in key mouse brain regions. These findings suggest potential neurotoxic risks associated with dietary intake of lectin-rich plant foods like bean sprouts.

Fibromyalgia (FM) is a widespread systemic pain disorder often accompanied by symptoms such as insomnia, mania, obesity, and depression. FM is difficult to diagnose and, therefore, cannot be effectively treated with current medical approaches. After prolonged suffering, FM patients frequently seek help from chronic pain physicians and psychiatrists. Eicosapentaenoic acid (EPA), derived from fish oil, is a common nutritional therapy for pain. While EPA is a documented fatty acid for depression treatment, its role in FM management is less established. In this study, we investigated the effects of EPA on FM pain and its potential mechanisms involving microglia/astrocytes and toll-like receptor 4 (TLR4) pathways in the cerebellum of mice. We found that intermittent cold stress (ICS) effectively induced FM-like pain in mice. Pain was evaluated using von Frey and Hargraves' tests to assess mechanical (2.01 ± 0.11 g) and thermal (4.09 ± 0.34 s) sensitivity. Nociceptive responses were alleviated by oral EPA administration (3.68 ± 0.13 g and 7.89 ± 0.3 s). EPA levels were lower in FM mice but increased following oral intake. Our findings revealed elevated levels of microglia/astrocyte markers and neurotransmitters such as HMGB1 and S100B in the cerebellum 5-7 (CB5-7) of FM mice. Similarly, TLR4 and related nociceptive signals were upregulated in the FM group. Notably, oral EPA effectively reduced these pain-related substances in CB5-7. Our results suggest that EPA can treat FM by modulating microglia/astrocyte activity and TLR4 signaling, highlighting its potential as a therapeutic target in FM management.

Background: To comprehensively evaluate the therapeutic potential of anthocyanins in animal models of Alzheimer's disease (AD).

Methods: The PubMed, Web of Science, and Embase databases were searched for preclinical animal studies investigating anthocyanin intervention in AD models up to June 2025. Studies reporting outcomes related to cognitive behavior, neuropathological changes such as amyloid-β (Aβ) deposition, or molecular mechanisms including oxidative stress and inflammatory markers, were included in the analysis. Data analysis was performed using RevMan 5.4 software. The SYRCLE tool was used to assess the risk of bia.

Results: Anthocyanin intervention significantly improved cognitive function in animal models of AD. Meta-analysis revealed that in the Morris water maze test, the anthocyanin treatment group exhibited a significantly higher number of crossings in the target quadrant compared to the control group (SMD = 1.83, 95% CI: 1.48 -2.18, p < 0.00001). Regarding pathological indicators, anthocyanin administration was associated with a significant reduction in Aβ protein deposition (SMD = -5.39, 95% CI: - 6.89 to - 3.88, p < 0.00001). Furthermore, anthocyanin effectively alleviated oxidative stress, as evidenced by a significant decrease in malondialdehyde (MDA) levels (SMD = -4.19, 95% CI: - 6.76 to - 1.63, p = 0.001). In terms of neuroinflammatory markers, anthocyanin treatment significantly reduced the expression levels of tumor necrosis factor-alpha (TNF-α) (SMD = -3.30, 95% CI: - 4.91 to - 1.68, p < 0.0001) and interleukin-1 beta (IL-1β) (SMD = -2.23, 95% CI: - 3.12 to - 1.34, p < 0.00001).

Conclusion: This systematic review and meta-analysis suggest that anthocyanins could improve cognitive function and mitigate neuropathology in animal models of AD.

Objectives: This review addresses dietary intervention for secondary stroke prevention. The review focuses on gut dysbiosis, innate and adaptive immune system, ischemic brain injury, proinflammatory cytokines, chemokines, mast cell degranulation, and blood brain barrier disruption.Methods: We investigated mitochondrial dysfunction, mast cells degranulation in conjunction with poststroke and alterations in gut microbiota. We discussed gut dysbiosis in conjunction with poststroke and the two-way gut-brain interactions. We evaluated the mechanisms underlying the involvement of dysbiosis in stroke and poststroke development including immune-mediated inflammatory responses, variation in blood-brain-barrier and intestinal barrier function, and reciprocal effects of microbial metabolites. We analyzed the nutrigenomic effects of the main cooking methods proposed for poststroke individuals and performed a comparative analysis of the nutrigenomic properties of the Mediterranean Diet and other Blue Zones healthy diets such as the Okinawa and Nordic diets.Results: Evidence in animals and humans is emerging about the interplay of gut microbiota before stroke including dysbiosis before stroke and stroke-induced dysbiosis. We proposed poststroke diet with dietary bioactive compounds from healthy plant-based foods, supplements, and appropriate cooking methods that will reestablish eubiosis and ameliorate the neurological and neuropsychiatric deficits in poststroke patients. Interventions to address the intersectionality of diet, gut microbiota and stroke and recommendations for food texture modifications in post-stroke dysphagia may help mitigate the downstream effects of acute and chronic inflammatory and immune damage.Discussion: The inclusion of dietary research intervention trials not limited to DASH, MIND, and the ongoing NOURISH trial may help further progress in the clinical treatment of stroke.