Nutritional Neuroscience最新文献

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.

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.

Background: Altered eating behaviors may precede the onset of full-scale eating disorders. Given the link between eating disorders and migraine, it is critical to identify individuals with migraine with altered eating behaviors. Therefore, this study aimed to investigate eating behaviors in a sample of migraine patients and to examine their potential associations with migraine frequency and related disability.

Methods: Adult patients diagnosed with migraine (n = 531) were asked to report their monthly migraine days (MMDs), complete the Headache Impact Test-6 (HIT-6), and answer the Adult Eating Behavior Questionnaire (AEBQ). A group of healthy controls (n = 1062) was also asked to answered AEBQ.

Results: Migraine patients had a significantly lower score in the enjoyment of food compared to controls (P = 0.037), whereas they had significantly higher scores in hunger and satiety responsiveness compared to controls (P values < 0.001 and 0.008, respectively). There were no statistically significant differences between patients and controls in terms of scores for food fussiness, food responsiveness, emotional overeating, slowness in eating, and emotional undereating. There were statistically significant negative correlations between MMDs and both enjoyment of food and food responsiveness scores (P = 0.006 and 0.032, respectively). A statistically significant positive correlation was found between HIT-6 total scores and satiety responsiveness scores (P = 0.002).

Conclusion: Altered eating habits are frequently reported among individuals with migraine, adding to the migraine burden. Health professionals, therefore, need to consider these eating behaviors to foster more tailored nutrition interventions for patients with migraine, aiming at improving their quality of life.

Objectives: The rising prevalence of cognitive decline linked to obesity is becoming a significant public health issue. Epidemiological studies indicate that a higher intake of fruits and vegetables (F&V) may be associated with a lower risk of cognitive impairment, although the evidence for the causal relationship is lacking. This study examined whether F&V supplementation could prevent cognitive decline in mice with high-fat diet-induced obesity.

Methods: Male C57BL/6J mice (6 weeks old) were randomly assigned to one of five diet groups (12 mice per group): low fat (LF, 10% kcal fat) diet, or high fat (HF0, 45% kcal fat) diet supplemented with 0% (HF0), 5% (HF5), 10% (HF10), or 15% (HF15) of a mixture of F&V (wt/wt). These levels of supplementation correspond to approximately 0, 3, 5-7, or 8-9 servings of F&V per day for humans, respectively. The novel object recognition test was performed after mice consumed the respective diets for 17 weeks.

Results: Mice fed the Western-style HF diet spent less time exploring the novel object, indicating significant cognitive impairment compared to the LF group. Conversely, F&V supplementation alleviated the HF diet-induced cognitive deficits in a dose-dependent manner.

Discussion: The results from this pilot study suggest the causal link between F&V intake and the prevention of cognition impairment caused by a Western-style high-fat diet, establishing a foundation for further investigation into the protective effects of F&V consumption on obesity-related cognitive decline. Additional research is required to better understand the underlying mechanisms.

Objectives: This review aims to evaluate the impact of food additives on brain tissue, focusing on oxidative stress-related mechanisms and their role in neurodegeneration.

Methods: A comprehensive literature search was conducted using PubMed, Scopus, Web of Science, ScienceDirect, and Springer, covering studies published up to 2025.

Results: Multiple studies indicate that food additives contribute to oxidative stress, leading to a decrease in glutathione (GSH) levels and superoxide dismutase (SOD) activity, while increasing malondialdehyde (MDA) concentrations in brain tissue. These biochemical changes are associated with inflammation and cellular damage.

Discussion: Findings suggest that certain food additives contribute to oxidative stress and other neurotoxic mechanisms, leading to cellular and molecular alterations in neural tissue, including functionally relevant brain regions. Further research is warranted to elucidate their long-term biological effects and inform regulatory decision-making.

Objectives: Exposure to elevated levels of fluoride from environmental or dietary sources can lead to toxic effects on the nervous system. This work examined the potential of hesperidin, a citrus-derived flavonoid recognized for its neuroprotective actions, to counteract NaF-induced toxicity in the rat cerebellum.

Methods: Male rats (n = 10 per group) were divided into four groups receiving either normal water, NaF (200 ppm) alone, NaF plus hesperidin (200 mg/kg/day), or hesperidin alone for 4 weeks. Neurobehavioral assessments, including the beam walking, ladder rung walking, inclined plane, and accelerating rotarod tests, were performed, followed by neurochemical and quantitative stereological analysis of the cerebellum.

Results: NaF-treated rats exhibited deficits in coordination, balance, learning, and adaptation as assessed by behavioral testing. However, co-treatment with hesperidin significantly prevented these motor deficits. Molecular findings indicated that hesperidin may have lessened NaF-induced neurotoxicity by helping to maintain brain-derived neurotrophic factor (BDNF) mRNA expression and preserving antioxidant enzyme activity [superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)], while simultaneously lowering malondialdehyde (MDA) levels and suppressing p53 expression. Stereological analysis showed that hesperidin prevented NaF-related reductions in total cerebellar, cortical, and white matter volumes, as well as in Purkinje cell number.

Discussion: Prolonged NaF exposure is linked to cerebellar structural alterations and motor deficits, likely mediated by oxidative stress, apoptosis, and disrupted neurotrophic signaling. In this experimental model, appeared to mitigate these effects by enhancing antioxidant defenses and supporting neuroprotective mechanisms, suggesting its potential to preserve cerebellar structure and function under fluoride-induced toxicity.