Nutritional Neuroscience最新文献

{"title":"Inhaled β-myrcene alleviates insomnia in mice by modulating 5-HT1A/PKA signaling and the gut microbiota.","authors":"Dawei Xu, Luge Chen, Xiaohu Chen, Weiming Jiang, Lijuan Sun","doi":"10.1080/1028415X.2026.2727956","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2727956","url":null,"abstract":"<p><strong>Background and objectives: </strong>Insomnia is a major public health issue that impairs daily functions and quality of life. Sleep-onset difficulty, a common complaint among patients, is accompanied by reduced central serotonin (5-HT) function. β-myrcene from lavender has sedative-hypnotic effects via serotonergic pathways, but most previous studies used intraperitoneal injection, which causes stress and limits clinical translation. Here, we asked whether non-invasive inhalation of β-myrcene produced similar effects in a mouse model of insomnia with low 5-HT function, and explored the underlying mechanisms.</p><p><strong>Methods: </strong>β-myrcene was given to PCPA-induced insomnia mice by inhalation (with intraperitoneal injection as a pharmacodynamic control). In the inhalation group, sleep and behavior were evaluated using the amobarbital sodium sleep test and spontaneous locomotor activity test. ELISA, RT-qPCR, Western blot, and 16S rRNA sequencing were applied to study mechanisms.</p><p><strong>Results: </strong>Inhaled β-myrcene shortened sleep latency and prolonged sleep duration. It also reduced oxidative stress and modulated GABA, 5-HT, and glutamate levels. These changes were accompanied by upregulation of mRNAs such as GABAARγ2 and 5-HT1A, as well as proteins including GAD65/67 and PKA, suggesting involvement of 5-HT1A/PKA signaling. Additionally, inhalation of β-myrcene was correlated with alterations in gut microbiota composition in PCPA-induced insomnia mice.</p><p><strong>Conclusions: </strong>Our findings indicate that inhaled β-myrcene is associated with sedative-hypnotic effects and alterations in gut microbiota composition in PCPA-induced insomnia mice, potentially involving modulation of 5-HT1A/PKA signaling.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-14"},"PeriodicalIF":3.1,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164412","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":"Syringic acid improves cognitive impairment in palmitic acid-induced obesity model: an <i>in vitro</i> and <i>in vivo</i> study.","authors":"Amina Khatun, Jayasree Saha, Priti Garai, Susovan Chowdhury, Surendra Patra, Ritobrata Goswami, Shrabani Pradhan, Kuntal Ghosh, Sudipta Chakrabarti","doi":"10.1080/1028415X.2026.2743239","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2743239","url":null,"abstract":"<p><strong>Objective: </strong>Obesity-mediated cognitive impairment is increasingly known as high levels of saturated fatty acid intake and accumulation in the body. Saturated fatty acids, mainly palmitic acid (PA) is recognized as the leading cause of oxidative stress, metabolic dysregulation, and neuronal degeneration in obesity.</p><p><strong>Method: </strong>The current study investigated the neuroprotective effects of syringic acid (SA) against PA-induced neuronal injury in N2a neuronal cells, as well as in a high-saturated-fat-induced obese mouse (DIO) model.</p><p><strong>Result: </strong>The study demonstrated that PA significantly reduced cell viability, increased lactate dehydrogenase release, nitric oxide generation, lipid peroxidation, reactive oxygen species, and intracellular lipid accumulation, following a decrease in the levels of glutathione, superoxide dismutase, catalase, and downregulation of synaptic plasticity-related molecules, including NR2a, PSD-95, and GluR1, in N2a neuronal cells. In high-saturated-fat-diet-induced mice, metabolic data showed a significant increase in body weight, basal metabolic rate, fasting blood glucose, and triglyceride levels, along with downregulation of synaptic plasticity and diminished behavioural activity. In contrast, SA treatment was able to restore cell viability and redox homeostasis by decreasing lipid peroxidation, LDH release, and NO generation, along with increasing GSH, SOD, and Catalase activity. It decreased ROS and lipid overload while maintaining neuronal morphology and synaptic molecule expression. The PPAR-α plays the main regulatory role in synaptic plasticity.</p><p><strong>Discussion: </strong>The <i>in vivo</i> study revealed that SA markedly decreased body weight, BMI, metabolic alteration, and upregulated synaptic plasticity. It improved spatial learning and memory in high-saturated-fat-induced mice. Together, these results illustrate that SA protects from neuronal dysfunction linked to obesity by means of antioxidant, anti-lipotoxic, and synaptic-plasticity-preserving mechanisms. Thus, SA might be a potential therapeutic target for cognitive impairment related to obesity and neurodegenerative disorders caused by overconsumption of saturated fats.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-22"},"PeriodicalIF":3.1,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137726","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 lysine deficiency impairs hippocampal-related functions and neurogenesis in rats.","authors":"Layal Jaafar, Rim Jaber, Alaa El-Makkawi, Christina Mary Kourie, Tamara Fahs, Maram Chaaban, Rami Arnaout, Carla El-Mallah, Batoul Darwish, Melhem Bilen, Omar Obeid, Wassim Abou-Kheir","doi":"10.1080/1028415X.2026.2742265","DOIUrl":"https://doi.org/10.1080/1028415X.2026.2742265","url":null,"abstract":"<p><strong>Background and objectives: </strong>Hippocampal neurogenesis enhances cognitive abilities and can be influenced by various dietary factors. Lysine, an essential amino acid, modulates neuronal activity and synaptic function; however, the impact of dietary lysine deficiency on neurogenesis remains unclear. This study investigated the effects of moderate and severe lysine deficiency on cognitive function, hippocampal neurogenesis, and gut microbiota composition in rats.</p><p><strong>Methods: </strong>Adolescent male Sprague-Dawley rats were assigned to three groups for four weeks: sham (adequate lysine), moderate (30%) lysine deficiency, or severe (60%) lysine deficiency. Body composition, body weight, and food intake were monitored weekly. Bromodeoxyuridine was administered at different time points to assess the proliferation and maturation phases of neurogenesis. Fecal samples were collected at the end of the study, and microbiota composition was characterized by 16S rRNA gene sequencing targeting the V3-V4 regions.</p><p><strong>Results: </strong>Body composition parameters were significantly impaired in the 60% lysine-deficient groups. Behavioral assessments showed that severe lysine deficiency was associated with altered anxiety-like and cognitive-related behaviors. Neurogenesis assessment revealed that both moderate and severe lysine deficiency reduced hippocampal neural stem cell proliferation, whereas differentiation was impaired only under severe deficiency. At the microbiota level, the 60% lysine-deficient group also showed the most pronounced alterations in gut microbial community composition, including reduced <i>Lactobacillus</i> species.</p><p><strong>Conclusion: </strong>Severe lysine deficiency was associated with impaired hippocampal neurogenesis, altered behavior, and gut microbiota composition, suggesting a potential gut-brain axis involvement, although causality remains to be established.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":3.1,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137730","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":"Naringenin ameliorates neuropsychiatric deficits in mice fed a methionine-choline-deficient diet.","authors":"Mohammad-Hadi Sahebi, Mohammad Nasehi, Azam Moslehi, Mohammad-Reza Zarrindast, Mohaddeseh Ebrahimi-Ghiri","doi":"10.1080/1028415X.2026.2641538","DOIUrl":"10.1080/1028415X.2026.2641538","url":null,"abstract":"<p><p>Neuropsychiatric dysfunction is increasingly being acknowledged as a disabling complication of non-alcoholic steatohepatitis (NASH), but there are no therapeutic approaches. We investigated in the present study the neuroprotective effectiveness of naringenin, a citrus flavonoid with known anti-inflammatory and neurotrophic effects, in a murine NASH model induced by an 8-week methionine-choline-deficient (MCD) diet. Male C57BL/6 mice (n = 8/group) were treated with naringenin (50 mg/kg/day, i.p.) during the final 4 weeks. In behavioral tests, naringenin counteracted cognitive impairment in novel object recognition, reduced anxiety in both open field and elevated plus maze paradigms, and decreased immobility in the forced swim test, indicating antidepressant-like activity. Mechanistically, naringenin restored hippocampal apoptotic balance, normalizing the MCD diet-induced <i>Bax</i> upregulation and <i>Bcl2</i> downregulation. Notably, while the MCD diet suppressed both <i>Bdnf</i> and <i>Ntrk2</i> expression, naringenin treatment partially restored <i>Bdnf</i> (but not <i>Ntrk2</i>) mRNA levels, implicating <i>Bdnf</i>-related neuroplasticity in its therapeutic effects. The research highlights naringenin's neuroprotective functions and its multitarget therapeutic potential in the MCD diet model of steatohepatitis, as evidenced by its effects on hippocampal gene expression and behavioral outcomes<i>.</i> Additional studies are needed to validate the effect in clinical settings and establish optimal dosing regimens.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1226-1238"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777228","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":"Chronotype and diet quality: mediating roles of stress, anxiety and depression in university students.","authors":"Sakshi Malik, Priyanka Srivastava","doi":"10.1080/1028415X.2026.2641539","DOIUrl":"10.1080/1028415X.2026.2641539","url":null,"abstract":"<p><strong>Background: </strong>Evening chronotype has been linked with depression and dietary behaviour. However, the mechanism that links circadian preference to diet quality in university students remains unclear. Psychological distress may mediate this pathway among university students prone to social jet lag.</p><p><strong>Objective: </strong>The present study investigates whether psychological distress mediates the association between chronotype and diet quality associations in university students, and to explore gender specific patterns.</p><p><strong>Methods: </strong>A cross-sectional study was conducted among 238 university students in Haryana, India (mean age-21.1 ± 3.15 years). The participants completed measures, including the Diet Quality Questionnaire (DQQ), the Morningness-Eveningness Scale, and the Depression, Anxiety, and Stress Scale-21 (DASS-21). The Generalised Linear Modelling with 1000 bootstrapped resamples to estimate the indirect and direct effects of chronotype on diet quality via stress, anxiety, and depression, with confidence intervals including gender-stratified analysis.</p><p><strong>Results: </strong>The findings report that evening chronotype was significantly associated with depression (β = -0.118, <i>p</i> = 0.031) at the component level, with the chronotype depression link being stronger in females, but directly associated with poor diet quality (β = 0.0828, <i>p</i> = 0.063). However, the indirect pathway was not significant, and all the bootstrapped confidence intervals for indirect effects had crossed zero in the total sample and by gender. The model explained 3.2% of the variance in diet quality.</p><p><strong>Conclusion: </strong>The study results indicate that sleep quality, together with light exposure, which the researchers did not measure in the research process, provides a better explanation for how chronotype affects students' dietary habits. The future studies should incorporate objective measures of sleep and daily light exposure.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1239-1250"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372994","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":"Nutritional intervention rich in tryptophan enhances sleep duration and reduces wakefulness during breast cancer treatment.","authors":"Henriqueta Vieira Van Keulen, Guilherme Eugênio Van Keulen, Jéssica Pereira Silva, Renato Moreira Nunes, Aline Silva Aguiar","doi":"10.1080/1028415X.2026.2650633","DOIUrl":"10.1080/1028415X.2026.2650633","url":null,"abstract":"<p><p><b>Background:</b> Sleep disorders are highly prevalent among women undergoing treatment for breast cancer, often exacerbated by the side effects of chemotherapy. Nutritional strategies using foods rich in tryptophan and precursors of melatonin may help regulate sleep, but evidence in cancer populations remains limited.<b>Objective:</b> To evaluate the effect of a tryptophan-rich dietary intervention on sleep parameters in women undergoing chemotherapy for breast cancer.<b>Methods:</b> Fifty women were randomized into a Sleep Diet Group (SDG) that received a tryptophan-rich meal plan (>3000 mg/day) or a Control Group (CG) that received a diet without specific foods to facilitate sleep. Sleep was monitored daily for six weeks using actigraphy (Mi Band 4C®), assessing total sleep time (TST), light sleep, deep sleep and wake after sleep onset (WASO). Fatigue and insomnia severity were assessed before and after the intervention.<b>Results:</b> The SDG had significantly higher TST compared to the CG in weeks 4 and 5 (p = 0.007 and p = 0.010, respectively). WASO was significantly lower in the SDG during weeks 2 and 4 (p = 0.011 and p = 0.035). No significant differences in deep sleep were observed between groups (p = 0.214). Both groups showed subjective improvements in insomnia severity, with no differences between groups. Fatigue scores remained unchanged.<b>Conclusion:</b> A dietary intervention with tryptophan-rich foods improved total sleep time and reduced nighttime awakenings in women undergoing breast cancer treatment. These findings suggest that targeted nutritional strategies may support sleep regulation during chemotherapy.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1268-1281"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777300","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":"Effect of vitamin E on cerebrovascular function: a systematic review.","authors":"Sarah Jansen, Coralie J Graham, Dean E Mills, Edward S Bliss","doi":"10.1080/1028415X.2026.2655229","DOIUrl":"10.1080/1028415X.2026.2655229","url":null,"abstract":"<p><p><b>Objectives:</b> Cerebrovascular function declines with normal ageing, and the antioxidant and anti-inflammatory properties of Vitamin E may maintain or improve this. The aim of this systematic review is to evaluate the effect of vitamin E on cerebrovascular function in both pre-clinical and clinical populations.<b>Methods:</b> Six databases (PubMed, MEDLINE, Web of Science, Scopus, ScienceDirect, and CINAHL) were searched in 2024 using keywords such as 'vitamin E', tocopherol, tocotrienol, 'cerebrovascular function', and related medical subject heading terms.<b>Results:</b> Of the 335 records returned, no clinical studies were identified. Ten pre-clinical studies met the inclusion criteria and were included for analysis. Due to heterogeneity in study designs and outcomes, a meta-analysis was not performed. Across animal models of cerebral ischaemia and haemorrhagic hypoperfusion, vitamin E supplementation improved cerebral blood flow, reduced intracranial pressure, and enhanced cerebrovascular responsiveness, thus reflecting improved cerebrovascular function. Furthermore, studies examining platelet aggregation reported delayed thrombus formation, likely mediated by reduced oxidative stress and improved endothelial function and nitric oxide bioavailability. However, with heterogeneous outcomes from pre-clinical studies and a lack of clinical studies, the translatability of data to the effect of chronic consumption on cerebrovascular function in humans is limited.<b>Discussion:</b> Pre-clinical data suggest that the antioxidant capacity of vitamin E and its regulatory effect on platelet aggregation may improve cerebrovascular function. However, the absence of clinical data limits translation to human populations. Future well-designed studies in older adults are warranted to determine whether vitamin E supplementation can preserve or improve cerebrovascular function throughout the ageing process.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1331-1345"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662971","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 multiple micronutrient supplementation on cognitive function in children: a systematic review and meta-analysis of randomized controlled trials.","authors":"Neda Asgari Avini, Hossein Shahinfar, Zahra Yazdian, Mahsa Ranjbar, Sakineh Shab-Bidar","doi":"10.1080/1028415X.2026.2650636","DOIUrl":"10.1080/1028415X.2026.2650636","url":null,"abstract":"<p><strong>Background: </strong>An updated and comprehensive understanding of the impact of multiple micronutrient (MMN) supplementation on cognitive function in children remains elusive. This study aimed to assess the effects of MMN supplementation on cognitive function in children under 18.</p><p><strong>Methods: </strong>We searched PubMed, Scopus, and WOS through May 11, 2025. Eligible randomized controlled trials in children and adolescents (≤18 years) comparing MMN supplementation (≥3 micronutrients) with placebo or control and assessing cognitive outcomes were included. Risk of bias was independently assessed by two reviewers using the Cochrane tool, with disagreements resolved by a third reviewer. Cognitive outcomes were divided into nine domains, and a meta-analysis using random-effects models was conducted.</p><p><strong>Results: </strong>Thirty-five studies met the inclusion criteria, with a total of 19,343 participants. Based on the RoB assessment, only four studies were classified as low risk. Our analysis showed a significant positive effect of supplementation on memory (SMD: 0.22; 95% CI: 0.08 to 0.35, <i>P</i> = 0.002) (<i>I</i>² = 73.8%, <i>P</i> < 0.000; GRADE: very low) and language (SMD: 0.09; 95% CI: 0.03 to 0.16, <i>P</i> = 0.006) (<i>I</i>² = 39.0, <i>P</i> = 0.067; GRADE: high). No significant effects were found in other cognitive domains.</p><p><strong>Conclusions: </strong>Overall, the meta-analysis suggests that the use of MMN supplements in children may result in slight improvements in language and memory domains. However, given the small effect sizes and considerable heterogeneity, the data are insufficient to support the regular intake of MMN for cognitive improvement in children.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1282-1315"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148144235","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":"Baru (<i>Dipteryx alata</i>) nut oil attenuates amyloid-β-induced cognitive deficits by modulating neuroinflammation and BDNF signaling pathway.","authors":"W C Martins, L R C Mendes, M C Junqueira, C M S Pereira, P C Gilbbert, S O Schommer, S S Campos, R de P C Rodrigues, V R P Santos, T M Brito, F Dobrachinski, E Lima, F Rios-Santos, S Vandresen-Filho","doi":"10.1080/1028415X.2026.2641534","DOIUrl":"10.1080/1028415X.2026.2641534","url":null,"abstract":"<p><p><b>Introduction:</b> Current treatments for Alzheimer's disease (AD) are primarily supportive and have limited efficacy in slowing disease progression. Therefore, the search for new therapeutic agents is essential to improve cognitive deficits or potentially prevent the advancement of this neurodegenerative disorder. <i>Baru oil (BO)</i> contains several bioactive compounds that may possess neuroprotective effects. However, no studies have investigated the potential beneficial effects of BO in the context of AD.<b>Aim and Methods:</b> This study aimed to investigate the neuroprotective effects of BO in a rodent model of AD. Mice were pretreated orally with vehicle or BO 1 or 3 g/kg/day for 45 days. On the 30th day, mice were infused i.c.v with amyloid-beta (Aβ) or PBS. A positive control group was orally treated with memantine (20mg/kg/day) for 15 days after Aβ or PBS infusion. Following behavioral assessments, mice were euthanized and the brains were removed for biochemical assays.<b>Results:</b> Similar to memantine treatment, pretreatment with both doses of BO prevented Aβ-induced memory impairments in the Morris water maze and the object recognition task. Pretreatment with BO 3g/kg/day prevented Aβ-induced increase in lipid peroxidation in the hippocampus. BO pretreatment mitigated the Aβ-induced reductions in hippocampal expression levels of BDNF, TrkB, and p-CREB. BO prevented the Aβ-induced increase in COX-2 and NOS-2 expression in the hippocampus.<b>Conclusion:</b> BO reversed Aβ-induced cognitive deficits. These neuroprotective effects were associated with the mitigation of hippocampal oxidative stress and neuroinflammation, alongside the restoration of the BDNF/TrkB/p-CREB signaling pathway. Our findings highlight Baru oil as a promising multifactorial therapeutic agent for AD.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1214-1225"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444528","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":"Interplay between serum vitamin D, irisin and galectin-3 in attention-deficit/hyperactivity disorder (ADHD).","authors":"Samson K Wilson, Mintu Mathew, Fasna Muhammed, R Bindu, Renjitha Bhaskaran, C Jayakumar, Jaya Thomas","doi":"10.1080/1028415X.2026.2651937","DOIUrl":"10.1080/1028415X.2026.2651937","url":null,"abstract":"<p><strong>Background: </strong>Vitamin D deficiency (VDD) has been widely studied for its role in attention-deficit/hyperactivity disorder (ADHD). Irisin is believed to act as a bridge between physical activity and cognition, while galectin-3 is involved in inflammation and immunity. Serum irisin and Galectin-3 levels are altered with vitamin D levels.</p><p><strong>Methods: </strong>A prospective case-control study was conducted to investigate the interplay between the serum levels of vitamin D, irisin and galectin-3 in South Indian children diagnosed with ADHD. We enrolled 152 children (<i>n</i> = 76 each in ADHD and healthy control) and evaluated their serum Vitamin D levels and estimated serum irisin and galectin-3 levels in a subpopulation of 70 children, among them (35 each in ADHD and matched controls).</p><p><strong>Results: </strong>VDD was more common in ADHD (<i>n</i> = 46; 60.5%) than in healthy controls (<i>n</i> = 22; 28.9%). Median serum vitamin D levels were significantly lower (16.99 (IQR 11.91-23.98) ng/mL) in ADHD than in controls (22.55 (IQR 18.92-28.81) ng/mL) (<i>p</i> < 0.001). Serum Irisin levels were lower, and galectin-3 levels were higher in ADHD than in healthy controls, although not statistically significant. Interestingly, there was a strong positive correlation between serum irisin and galectin-3 in ADHD (<i>r</i> = 0.707, <i>p</i> < 0.001), while the correlation was weak in controls (r = 0.336, <i>p</i> value 0.049).</p><p><strong>Conclusion: </strong>The high prevalence of VDD in ADHD implies the importance of vitamin D and its proper monitoring. The strong positive correlation between irisin and galectin-3 in ADHD highlights the possibility of the irisin-galectin-3 duo serving as a potential biomarker in ADHD, subject to confirmation in a larger population.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1316-1330"},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948749","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}