Nutritional Neuroscience最新文献

{"title":"Sweetness exposure modulates brain networks in children responding to sucrose solutions: a functional MRI study.","authors":"Chun-Wei Hsu, Camille Divert, Daniel Grucker, Sophie Nicklaus, Luc Marlier","doi":"10.1080/1028415X.2025.2608367","DOIUrl":"10.1080/1028415X.2025.2608367","url":null,"abstract":"<p><strong>Context: </strong>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.</p><p><strong>Method: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"849-866"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vanillic acid protects against lead-induced cognitive impairment and neurodegeneration via GFAP/NRF-2 pathways in rats.","authors":"Ogunlade Babatunde, Kingsley Afoke Iteire, Sunday Aderemi Adelakun, Tolulope Judah Gbayisomore","doi":"10.1080/1028415X.2025.2608843","DOIUrl":"10.1080/1028415X.2025.2608843","url":null,"abstract":"<p><p><b>ABSTRACT</b><b>Objectives:</b> 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) (<i>n</i> = 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 (<i>n</i> = 6, per group) and ketamine anesthesia + perfusion (<i>n</i> = 4 per group). The brains were dissected and processed for histological, biochemical, and immunohistochemistry studies. <b>Results:</b> 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. <b>Discussion:</b> VA shows protective effects against LA-induced neurodegeneration and cognitive impairment suggesting a therapeutic role in heavy metal neurotoxicity.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"886-908"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145912569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of probiotics BB-12 and Bifico on radiation-induced brain injury, cognitive dysfunction and gut microbiota composition.","authors":"Shan Yang, Huake Yang, Bin Wang, Wen Guo, Wei Wang, Yunhe Ding, Wei Wang, Xilong Xie, Yafeng Ji, Feng Liu, Daimin Xiang, Mengmeng Ren, Bo Zhang, Xiaojin Wu, Gaolei Ma","doi":"10.1080/1028415X.2025.2595176","DOIUrl":"10.1080/1028415X.2025.2595176","url":null,"abstract":"<p><strong>Background: </strong>Whole brain irradiation (WBI) is an essential treatment for brain tumors and metastases, but often leads to radiation-induced brain injury (RIBI), and cognitive dysfunction, significantly impairing patients' quality of life. Emerging evidence highlights the role of gut microbiota dysbiosis in neurological disorders via the microbiota-gut-brain axis (MGBA). This study investigated the neuroprotective effects of probiotics Bifidobacterium animalis subsp. lactis BB-12 (BB-12) and Bifico on WBI-induced cognitive impairment in mice.</p><p><strong>Methods and results: </strong>After 4 weeks of BB-12 and Bifico intervention, the cognitive performance of WBI mice in Y-maze and Morris water maze (MWM) tests improved significantly. The interventions also mitigated impairments in hippocampal neurogenesis, reduced the overactivation of microglia and astrocytes, and alleviated neuroinflammation. 16S rRNA sequencing revealed that WBI-induced gut microbiota dysbiosis, characterized by reduced alpha diversity and increased Helicobacter abundance, was reversed by probiotic treatment. Additionally, BB-12 and Bifico restored intestinal barrier integrity, as indicated by upregulated tight junction proteins, and reduced colonic and systemic inflammation.</p><p><strong>Conclusion: </strong>This study suggests that probiotics BB-12 and Bifico promote recovery from RIBI and cognitive dysfunction by modulating the MGBA, providing new insights into potential strategies for intervening in RIBI and cognitive dysfunction.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"794-815"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148043092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthy-Unhealthy food group balance and cognitive performance in Chilean adolescents: a canonical correlation analysis - The Cogni-Action Project.","authors":"Humberto Peña-Jorquera, Alexis Díaz-Bahamondes, Natalia Quijada-Mateluna, Lara Carneiro, Mara C Lofrano-Prado, Gerson Ferrari, José Francisco López-Gil, Carlos Cristi-Montero","doi":"10.1080/1028415X.2026.2693299","DOIUrl":"10.1080/1028415X.2026.2693299","url":null,"abstract":"<p><strong>Background: </strong>While associations between individual nutrients and cognitive performance are well documented, the joint influence of healthy and unhealthy food group combinations on cognition remains poorly understood. This study examined whether the balance between healthy and unhealthy food group intake is associated with cognitive performance in youth, using a multivariate, pattern-based analytical approach.</p><p><strong>Methods: </strong>This cross-sectional study included 1,296 Chilean children and adolescents (10-14 years; 50% girls). Cognitive performance was assessed using eight standardized neurocognitive tasks, and dietary intake was evaluated using the Global Food Quality Index. Linear regression models were used to explore associations between individual food groups and cognitive outcomes, with correction for multiple testing. Canonical correlation analysis (CCA) was applied to identify multivariate modes of covariation between food group intake patterns and cognitive performance. Sex-stratified analyses were exploratory.</p><p><strong>Results: </strong>The CCA identified a significant mode of covariation in the full sample (rc = 0.25, <i>p</i> = .027). Cross-loadings indicated that a dietary configuration characterized by higher consumption of legumes and fish, together with lower intake of pastries, soft drinks, and fried foods, was associated with greater performance across most cognitive tasks (7 of 8), including fluid intelligence and processing speed, except for reverse memory span. No robust multivariate patterns were observed in sex-stratified analyses.</p><p><strong>Conclusion: </strong>The balance between healthy and unhealthy food group intake, rather than isolated food choices, is associated with cognitive performance in children and adolescents. Considering overall dietary configurations may provide a more informative framework for understanding diet-cognition relationships during this critical developmental period.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-13"},"PeriodicalIF":3.1,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148331742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbial modulation of CNS remyelination in multiple sclerosis: the missing link in gut-brain axis research.","authors":"Mingzhu Li, Peng Sun, Xiaojing Zhou, Ximeng Yang, Wen Li","doi":"10.1080/1028415X.2026.2686736","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2686736","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a chronic, immune-mediated disorder of the central nervous system (CNS) marked by demyelination and neurodegeneration. While much attention has focused on immune dysregulation and neuroinflammation, the failure of effective remyelination is a key driver of disease progression, especially in progressive MS. Recently, the gut microbiome has emerged as a potent modulator of systemic immunity and CNS function, influencing processes such as neuroinflammation and neurogenesis. This review examines current evidence on microbiota-derived metabolites, including short-chain fatty acids (SCFAs), indole derivatives, and bile acids, and their potential roles in pathways associated with oligodendrocyte precursor cell (OPC) biology and remyelination. Evidence from preclinical models, including germ-free systems, fecal microbiota transplantation (FMT), and probiotic interventions, suggests that microbial signals can modulate immune responses and CNS environments that may indirectly affect demyelination and repair processes. However, direct causal effects on OPC differentiation and functional remyelination remain incompletely established. We critically evaluate the strengths and limitations of existing studies, highlighting inconsistencies across experimental models and the context-dependent nature of microbiota-host interactions. Clinical evidence remains limited, with current studies primarily assessing inflammatory or metabolic outcomes rather than direct measures of remyelination. Key translational challenges include uncertainties regarding metabolite bioavailability in the CNS, cell-specific mechanisms of action, and reproducibility of microbiome-targeted interventions.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":3.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review on thymoquinone: a promising therapeutic molecule in Alzheimer's.","authors":"Simran Deep Kaur, Varun Singh, Hemlata Kaurav, Sopan Nangare, Samar Vihal","doi":"10.1080/1028415X.2026.2682949","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2682949","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory loss, cognitive decline, amyloid-<math><mi>β</mi></math> deposition, tau pathology, oxidative stress, and neuroinflammation. Thymoquinone (TQ), the principal bioactive constituent of <i>Nigella sativa (NS)</i>, has emerged as a promising candidate for AD management because of its neuroprotective properties. This review summarizes current evidence on the therapeutic potential of TQ in AD, with emphasis on its antioxidant, anti-inflammatory, anti-amyloid, anti-tau, and cholinergic-modulating actions. Experimental studies indicate that TQ can reduce oxidative damage, suppress NF-<math><mi>κ</mi></math>B- and TLR-associated inflammatory signaling, limit amyloid-<math><mi>β</mi></math> accumulation, modulate tau-related pathology, and improve neuronal survival and cognitive performance in several AD models. The review also discusses delivery strategies to improve the bioavailability and brain targeting of TQ, including nanoformulation-based approaches. Although the available pre-clinical findings support the therapeutic promise of TQ. The well-designed clinical studies are required to establish its efficacy, safety, optimal dosing, and long-term translational value in treating AD.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":3.6,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary habits and olfactory function in individuals with Parkinson's disease: an underexplored association.","authors":"Henrique José Cavalcanti Bezerra Gouveia, Shalini Balaji Vilvanathan, Johannes Frasnelli","doi":"10.1080/1028415X.2026.2684652","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2684652","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurological disorder characterized by motor and non-motor symptoms, including olfactory dysfunction, which may precede motor manifestations by up to 10-20 years. Given the role of olfaction in flavor perception and dietary behavior, olfactory impairment may significantly affect nutritional status and quality of life in individuals with PD. This opinion article discusses the relationship between olfactory dysfunction and dietary habits in PD, highlighting the scarcity and inconsistency of the available evidence. While some studies suggest that lower diet quality and reduced intake of specific nutrients are associated with worse olfactory performance, others found no significant correlations. We argue that these inconsistencies largely reflect methodological limitations. Future studies should adopt supervised data collection, validated olfactory tests, and culturally adapted dietary tools. Clarifying whether specific dietary patterns influence olfactory performance or whether olfactory impairment drives inappropriate eating behaviors is essential for better understanding disease progression and informing clinical strategies aimed at improving symptoms, nutritional status, and quality of life in people living with PD.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-5"},"PeriodicalIF":3.6,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine attenuates SPS-induced cognitive and affective deficits and corticolimbic injury in Wistar rats via restoration of BDNF and redox-inflammatory balance.","authors":"Godson Emeka Anyanwu, Precious E Ekwueme, Ayugha Nsan, Lilian Ezeugwu, Prisca Chiamaka Ogbe, Chinyere N Anyanwu, Vivian O Ojiakor, Chima Paul Okechukwu Ugwu","doi":"10.1080/1028415X.2026.2684552","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2684552","url":null,"abstract":"<p><strong>Background: </strong>Single prolonged stress (SPS) is a validated PTSD-like paradigm that causes cognitive and affective dysfunction and corticolimbic injuries due to the dysregulation of the HPA-axis and neurotrophic, redox, and neuroimmune pathways. Berberine is a bioactive isoquinoline alkaloid that demonstrates neuroprotective effects, although its effect on corticolimbic-pathology caused by SPS is yet to be fully characterized.</p><p><strong>Objectives: </strong>To ascertain whether berberine attenuates SPS-induced neurobehavioral impairments and corticolimbic neuronal damage in Wistar rats.</p><p><strong>Methods: </strong>Adult male Wistar rats were exposed to SPS (restraint, forced swim, and anesthetic-induced loss of consciousness) and left undisturbed for 7 days to allow stress consolidation. Then, rats were given oral berberine (50 or 200 mg/kg) or fluoxetine (10 mg/kg) in a single daily dose. Behavioral measures were Y-maze spontaneous alternation, Morris water maze, novel object recognition and sucrose preference. ELISA was used to quantify serum corticosterone. BDNF, SOD, catalase, MDA, and IL-1b/IL-6/TNF-a were assayed in the hippocampus and mPFC. CFV and NeuN immunohistochemistry were used to assess neuronal integrity and astrocytic reactivity was assessed using GFAP-immunoreactivity.</p><p><strong>Results: </strong>SPS induced severe deficits in working memory, spatial and recognition memories and reward sensitivity, and high basal corticosterone. It increased lipid peroxidation and pro-inflammatory cytokines while reducing antioxidant enzyme activities in brain tissue homogenates (hippocampus and medial prefrontal cortex). Berberine improved behavioral outcomes and attenuated endocrine, biochemical, and histopathological abnormalities in a dose-dependent manner.</p><p><strong>Conclusion: </strong>Berberine attenuates SPS-induced-cognitive/affective dysfunction and corticolimbic-lesion and establishes normalization of basal corticosterone, BDNF recovery, antioxidant defense, lipid peroxidation, cytokine elevations, and astrocytic activation. These findings support berberine as a multi-target candidate for mitigating stress-related-neurotoxicity.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-19"},"PeriodicalIF":3.6,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148205671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eicosapentaenoic acid intake modulates programmed cell death protein 1 receptors to prevent chronic pain and comorbid depression in mice.","authors":"Chien-Yi Ho, Younbyoung Chae, I-Han Hsiao, Ming-Chia Lin, Hsien-Yin Liao, Kuan-Pin Su, Hsin-Cheng Hsu, Yi-Wen Lin","doi":"10.1080/1028415X.2026.2678479","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2678479","url":null,"abstract":"<p><strong>Background: </strong>Fibromyalgia is a frequently treatment-refractory chronic musculoskeletal pain disorder that often results in clinical depression; however, the role of neuroinflammatory signaling in comorbid depression remains unclear, including the contributions of anti-inflammatory omega-3 fatty acids like eicosapentaenoic acid (EPA).</p><p><strong>Methods: </strong>This study examined the efficacy of EPA ingestion for reducing chronic pain and depression comorbidity (CPDC) in a mouse model established using intermittent cold stress.</p><p><strong>Results: </strong>Our results showed that oral EPA could alleviate mechanical and thermal hyperalgesia in CPDC mice. The preventive effect of EPA on depressive symptoms in CPDC mice was further confirmed. Western blot and immunofluorescence staining revealed that EPA can inhibit the enhanced neuroinflammatory signaling concomitant with increased astrocyte and microglia activation and elevated levels of inflammatory signaling factors high-mobility group box 1 (HMGB1) and S100B in the CPDC mice. Alternatively, oral EPA can increase the attenuated expression of the pain-inhibiting programmed cell death protein 1 (PD-1) receptor. EPA intake can further alleviate inflammation-associated toll-like receptor 4 (TLR4) and downstream signaling molecules myeloid differentiation primary response 88 (MyD88), TNF receptor associated factor 6 (TRAF6), and activated (phosphorylated) nuclear factor kappa-light-chain-enhancer of activated B cells (pNFκB) in CPDC mouse brain. A similar response also observed in <i>transient receptor potential vanilloid 1</i> gene knockout mice.</p><p><strong>Conclusion: </strong>This demonstration that oral EPA can prevent CPDC by inhibiting neuroinflammatory pathways could facilitate improved treatment strategies for CPDC.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-17"},"PeriodicalIF":3.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLP-1 receptor agonists in neuroinflammation: a novel therapeutic target?","authors":"Paula Brielle Pontes Silva, Raul Manhães de Castro, Joaci Pereira Dos Santos Junior, Henrique José Cavalcante Gouveia, Ana Elisa Toscano","doi":"10.1080/1028415X.2026.2680999","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2680999","url":null,"abstract":"","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-3"},"PeriodicalIF":3.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148157136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}