Neuroscience最新文献

{"title":"Chemogenetic re-activation of a neuronal ensemble in the lateral hypothalamus that is active during activity-based anorexia in mice modulates feeding and running activity","authors":"Erik Schéle ,&nbsp;Iris Stoltenborg ,&nbsp;Renée Poelman ,&nbsp;Roger A.H. Adan ,&nbsp;Suzanne L. Dickson","doi":"10.1016/j.neuroscience.2025.06.006","DOIUrl":"10.1016/j.neuroscience.2025.06.006","url":null,"abstract":"<div><div>A high level of physical activity is common in patients with anorexia nervosa and can exacerbate symptoms and recovery prognosis. The underlying cause is not known but is most likely regulated by the brain and may derive from energy deficit. Numerous brain regions are activated by energy deficit, and here we identify the lateral hypothalamus (LH) as one of those brain regions by mapping and chemogenetically controlling activated neurons in this area in the activity-based anorexia (ABA) mouse model. Our studies employing the Fos-TRAP2 technique revealed an increased number of activated neurons in the LH and in the lateral septum (LS) of female ABA mice compared to <em>ad libitum</em> fed running controls. Re-activation of these ABA-induced neuronal ensembles in the LH, but not LS, increased both feeding and locomotor activity. Additionally, chemogenetic inhibition decreased both behaviours. These findings suggest that the LH (but not the LS) under energy deficit is an important brain region that controls feeding and excessive running activity in the ABA model.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"580 ","pages":"Pages 35-45"},"PeriodicalIF":2.9,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative role of diet and gut microbiome dynamics for the Interventive therapeutics of Spinocerebellar ataxia type 3: The Current Update.","authors":"Ankita Singh, Jiya Bansal, Aakanksha Bharti, Meenu Joshi, Chakkaravarthi Saravanan, Chakresh Kumar Jain","doi":"10.1016/j.neuroscience.2025.06.024","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.06.024","url":null,"abstract":"<p><p>Neurodegenerative disorders such as Alzheimer's and Parkinson's have captured researchers' attention regarding their connection to gut microbiota and dietary factors. Research has shown that changes in our regular dietary consumption can profoundly influence the composition of the gut microbiota, which possesses the capacity to influence brain functioning through a number of mechanisms, suggesting that dietary modifications may serve as promising therapeutic intervention for managing and potentially mitigating the progression of several neurodegenerative diseases. Spinocerebellar Ataxia Type 3 (SCA3), a neurodegenerative disorder stems from an unstable CAG trinucleotide repeat expansion within the ATXN3 gene's coding regions. This leads to the production of polyglutamine, contributing to a range of symptoms. However, the therapeutic potential of targeting gut microbiome alterations through dietary interventions for SCA3 has not been extensively investigated. This review is the first to systematically integrate existing evidence on how dietary interventions and gut microbiome dynamics may be leveraged for the therapeutic management of SCA3. Specifically, we explore how dietary components including fermented foods, probiotics, fiber-rich diets, herbal compounds and pharmacological agents, including dietary and natural HDAC inhibitors can influence gut microbiota and modulate neuroinflammation, oxidative stress, and protein aggregation, which are common hallmarks in neurodegenerative diseases. This paper elucidates the gut microbiota's ability to affect neurological health and its significance in the management of SCA3, hence facilitating future research aimed at treating SCA3 patients by dietary modifications that modify particular gut flora.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokine CCL12 in trigeminal ganglion contributes to CFA-induced mechanical allodynia in mice","authors":"Xiaoxia Ma ,&nbsp;Lijia Mai ,&nbsp;Yifan He ,&nbsp;Shilin Jia ,&nbsp;Ruihan Yang ,&nbsp;Wenguo Fan ,&nbsp;Fang Huang","doi":"10.1016/j.neuroscience.2025.06.026","DOIUrl":"10.1016/j.neuroscience.2025.06.026","url":null,"abstract":"<div><div>Chemokines are known to play a role in the nervous system, involving a wide range of functions including the development of chronic pain. The C–C motif chemokine ligand 12 (CCL12) and its receptor CCR2 have been implicated in the pathophysiology of chronic pian. However, the precise mechanisms by which CCL12 influences the development and persistence of pain remain unclear. In this study, we aim to investigate the roles of CCL12 in chronic inflammatory pain at the primary sensory ganglion level. A mouse model of orofacial pain was established by subcutaneous injection of complete Freud’s adjuvant (CFA) into the right whisker pad. Mechanical allodynia was assessed using the von Frey test. The expression of CCL12 in the trigeminal ganglion (TG) was markedly upregulated at 7 days post-injection (dpi). Immunofluorescence and single-cell RNA-sequencing (scRNA-seq) data revealed that CCR2 was predominantly expressed in macrophages in the TG following CFA injection. To specifically target CCL12, an interfering adeno-associated virus (AAV) was administered intraganglionically into the right TG. Knockdown of <em>Ccl12</em> in the TG significantly alleviated mechanical allodynia and c-Fos expression in the spinal trigeminal nucleus caudalis (SpVc) of CFA mice. Additionally, the infiltration of macrophages and the levels of IL-6 and TNF-α in the TG were significantly increased at 7 dpi and were attenuated by <em>Ccl12</em> knockdown. These findings suggest that CCL12 contributes to CFA-induced orofacial allodynia by promoting macrophage infiltration and the production of IL-6 and TNF-α in the TG<strong>.</strong></div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"580 ","pages":"Pages 115-123"},"PeriodicalIF":2.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum albumin and total bilirubin are associated with poor outcomes in patients with acute ischemic stroke","authors":"Chanjuan Wei ,&nbsp;Ying Yang ,&nbsp;Yahui Hu,&nbsp;Xiaoshuang Xia,&nbsp;Wenjun Feng,&nbsp;Xin Li","doi":"10.1016/j.neuroscience.2025.06.010","DOIUrl":"10.1016/j.neuroscience.2025.06.010","url":null,"abstract":"<div><h3>Background</h3><div>Few studies have investigated the correlation between serum liver function indices and clinical outcomes in acute ischemic stroke (AIS) patients.</div></div><div><h3>Methods</h3><div>Patients with AIS from January 2020 to March 2023 were retrospectively analyzed. The clinical outcomes included stroke severity at admission and poor prognosis at discharge and 3 months. Multivariate logistic regression was used to evaluate the associations of liver function indicators with risk and adverse outcomes. Subgroup analysis was conducted to explore the relationships between liver function indices and clinical outcomes. The predictive value of these indices for adverse outcomes was assessed via receiver operating characteristic (ROC) curves.</div></div><div><h3>Results</h3><div>A total of 2022 AIS patients were included in this study. After adjustment for confounding factors, lower albumin levels were associated with higher NIHSS scores at admission (OR = 0.924, <em>95 % CI</em>: 0.901–0.947) and poor functional outcomes at discharge (OR = 0.950, <em>95 % CI</em>: 0.920–0.981) and at 3 months (OR = 0.913, <em>95 % CI</em>: 0.878–0.950). Similarly, higher total bilirubin levels were also correlated with higher baseline NIHSS scores (OR = 1.038, <em>95 % CI</em>: 1.022–1.055) and poor functional outcomes at discharge (OR = 1.021, <em>95 % CI</em>: 1.001–1.042) and at 3 months (OR = 1.029, <em>95 % CI</em>: 1.004–1.054). The risk of a poor 3-month prognosis in AIS patients increased with decreasing albumin levels at admission, independent of age, sex, and history of stroke (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusions</h3><div>Decreased ALB and increased total bilirubin levels were associated with increased NIHSS scores at admission and poor prognosis at discharge and 3 months in AIS patients.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 321-328"},"PeriodicalIF":2.9,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disturbed neurovascular coupling of limbic system in obstructive sleep apnea patients with mild cognitive impairment: A combined fMRI and ASL study.","authors":"Qiang Huang, Yun Yang, Hongwei Ma, Xiangbo Yan, Yi Wang, Jing Su, Qing Zhang","doi":"10.1016/j.neuroscience.2025.06.013","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.06.013","url":null,"abstract":"<p><p>Obstructive sleep apnea (OSA) is a common sleep disorder that causes long-term intermittent hypoxia and sleep disturbances, negatively affecting cognitive function. The mechanisms underlying cognitive impairment in OSA may involve alterations in both brain structure and function. This study investigates the potential role of disturbed neurovascular coupling (NVC) in cognitive decline among OSA patients. A total of 27 OSA patients with mild cognitive impairment (OSA-MCI) and 26 with normal cognitive function (OSA-NC) were included. We calculated the correlation coefficients for z-transformed amplitude of low-frequency fluctuations (ALFF) and cerebral blood flow (CBF) at global and regional brain voxel levels using resting-state functional magnetic resonance imaging (rs-fMRI) and arterial spin labeling (ASL) to assess NVC. General linear modeling and partial correlation analysis revealed that OSA-MCI patients exhibited disturbed NVC primarily within the limbic system, which was associated with cognitive decline. The ROC curve demonstrated that left hippocampus exhibited the highest classification performance in distinguishing between two groups. In conclusion, this study highlights a strong association between disturbed NVC and cognitive decline in OSA, and underscore the potential of NVC as a biomarker for early detection and intervention in OSA-related cognitive impairment.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144294149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-ictal causal connectivity reveals the epileptic network characteristics for deep brain stimulation","authors":"Yifan Wang ,&nbsp;Tao Yu ,&nbsp;Yulan Ma ,&nbsp;Weigang Cui ,&nbsp;Xueyuan Wang ,&nbsp;Liankun Ren ,&nbsp;Yang Li","doi":"10.1016/j.neuroscience.2025.06.025","DOIUrl":"10.1016/j.neuroscience.2025.06.025","url":null,"abstract":"<div><div>Deep brain stimulation of anterior nucleus of the thalamus (ANT-DBS) is an effective clinical treatment for drug-resistant focal epilepsy. However, the complex epileptic network characteristics underlying ANT-stimulation effectiveness remain unknown, owing to currently unclear connectivity between ANT and seizure-related cortex in pre-ictal periods. Here, we developed a novel individualized pre-ictal ANT-cortical tripartite connectivity network (PANT-CTCNet), aiming to reveal epileptic network characteristics using intracranial stereo-electroencephalography (sEEG) recordings in five patients with focal epilepsy for 90 trials. Each trial represented a pre-ictal or post-stimulus sEEG duration, which was used to construct the epileptic network. By employing conditional Granger causality, we constructed individualized ANT-cortical connectivity networks and found a common epileptic network centred on ANT closely connected with seizure-related cortex in pre-ictal periods. After ANT stimulation for clinical validation, strengthened pre-ictal connectivity between ANT and epileptogenic zones led to significant decline in the causal intensity of epileptic networks. The PANT-CTCNet can give a quantitative reference for clinical preoperative evaluation of patient suitability for ANT-DBS treatment. These findings regarding epileptic network characteristics provide theoretical basis in the selection of optimal surgical candidates for personalized ANT-DBS.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 329-343"},"PeriodicalIF":2.9,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ML184 influences coping strategies via GPR55-dependent mechanisms following its delivery in the periaqueductal gray (PAG) region","authors":"Carlos H. López-Lariz,&nbsp;Bruno A. Marichal-Cancino","doi":"10.1016/j.neuroscience.2025.06.016","DOIUrl":"10.1016/j.neuroscience.2025.06.016","url":null,"abstract":"<div><div>GPR55 is a cannabinoid and lysophospholipid-related receptor involved in multiple functions in the mammalian central nervous system (CNS). In the periaqueductal gray (PAG), GPR55 participates in pain integration, anxiety-related behaviors, and alcohol intake. In this study, ML184 (a synthetic GPR55 agonist) was injected into the PAG region in the absence and presence of CID16020046 (a selective GPR55 antagonist) to analyze the role of GPR55 in anxiety, exploration, and coping responses. Admittedly, the exact areas affected by the drug delivery were not confirmed. Hence, the drugs might have spread to adjacent PAG regions. In the open field (OF) test, ML184 and CID16020046 showed no significant effects (p &gt; 0.05 vs. vehicle) in all parameters tested, but the combination ML184 + CID16020046 increased rearing (p &lt; 0.05). In the elevated plus maze (EPM) test, ML184 and CID16020046 lack an effect (p &gt; 0.05 vs. vehicle) in all parameters tested. In contrast, the combination ML184 + CID16020046 increased time and distance in open arms (p &lt; 0.05). In the defensive burying behavior (DBB) test, CID16020046 produced no effects in all parameters tested (p &gt; 0.05 vs. vehicle). However, ML184 increased freezing and decreased pile height, time in motion, and bury ratio (p &lt; 0.05). All those actions were prevented with CID16020046-pretreatment. Our results suggest that GPR55 in PAG and/or its surrounding regions promote passive coping responses. Moreover, ML184 may induce anxiolytic effects and higher-rearing behaviors by GPR55-independent mechanisms (which remain to be identified).</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"580 ","pages":"Pages 71-79"},"PeriodicalIF":2.9,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating acupuncture therapy in depression: mechanisms of synaptic plasticity regulation","authors":"Yuxin Si ,&nbsp;Weigang Ma ,&nbsp;Qingxiang Zhang ,&nbsp;Youlin Zhang ,&nbsp;Jiaying An ,&nbsp;Miao Zhang ,&nbsp;Yu Fu ,&nbsp;Yujie Yu ,&nbsp;Han Zhang ,&nbsp;Yuxin Fang ,&nbsp;Di Zhang","doi":"10.1016/j.neuroscience.2025.06.005","DOIUrl":"10.1016/j.neuroscience.2025.06.005","url":null,"abstract":"<div><div>Depression is a severe heterogeneous mental illness that is highly co-morbid with other mental and somatic disorders. It poses a significant healthcare burden on both individuals and society. Currently, the use of single-target antidepressants exhibits suboptimal efficacy with significant adverse effects. Acupuncture has been advocated as a practical and effective treatment for depression, due to its low adverse effects rate compared to antidepressant medication. Currently, several studies have shown that acupuncture treatment for depression primarily involves multiple therapeutic mechanisms, including the regulation of specific gene expression, neuropeptide and neurotransmitter release, increasing the expression of neurotrophic factors, suppressing hyperactivity of the hypothalamic–pituitary–adrenal (HPA) axis, attenuating inflammatory responses, and restoring gut microbiota balance. These therapeutic effects involve the regulation of critical signaling pathways, including the cAMP-responsive element binding protein (CREB) signaling pathway, mitogen-activated protein kinases (MAPK) signaling pathway, mechanistic target of rapamycin (mTOR) signaling pathway, and toll-like receptors (TLR) signaling pathway. Notably, depression-associated molecular mechanisms and signaling pathway dysregulations are closely linked to impaired neural and synaptic plasticity. Acupuncture synergistically modulates the neuro-immune-microbiome multidimensional network and integrates crosstalk among key pathways such as CREB, thereby systemically restoring synaptic plasticity. This multi-dimensional integrative mechanism likely underlies its therapeutic superiority over single-target antidepressants. This review aims to elucidate how acupuncture restores cerebral synaptic plasticity by rectifying depression-related systemic dysfunctions and signaling pathway abnormalities, which will advance our understanding of its regulatory potential in depression treatment and inform the development of precision therapeutic strategies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 284-301"},"PeriodicalIF":2.9,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144280635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxic sprays, fragile brains: assessing pesticides exposure and disparities on neurodevelopment","authors":"Salma Mowafi ,&nbsp;Areeg M. Dabbish ,&nbsp;Chisom Cynthia Chukwuma ,&nbsp;Lobna Adel ,&nbsp;Anwar Abdelnaser","doi":"10.1016/j.neuroscience.2025.06.021","DOIUrl":"10.1016/j.neuroscience.2025.06.021","url":null,"abstract":"<div><div>Pesticides are widely used for agricultural and domestic purposes. However, their use raises concerns about potential health risks, especially for vulnerable populations like children and their neurodevelopment. This review highlights the common routes of pesticide exposure for children, the consequences of the exposure period on neurodevelopmental disorders, the possible epigenetic modifications of these pesticides, and the disparities in exposure. Common routes of exposure include oral ingestion, proximity to application sites, and prenatal exposure. There is a strong association between exposure to certain pesticides, like organophosphates, organochlorines, and pyrethroids, with autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), and impairments in cognitive function. The timing of pesticide exposure plays a key role in determining the severity of neurodevelopmental outcomes: prenatal exposure to pesticides was most critical, especially during the first and third trimesters, while postnatal exposure, especially in early childhood, also increased risks, particularly for ADHD. Prenatal exposure to organophosphates and carbamates alter the standard cellular mechanisms and mitochondrial functions. Exposure to pyrethroids and organophosphates was also associated with cognitive impairment in children with permutation of the Fragile X Messenger Ribonucleoprotein gene. We highlight the disparity in pesticide exposure across various populations, such as those from lower socio-economic backgrounds and minority communities. We emphasize that the impact of pesticides is not solely biological; the interplay of social and environmental factors also influences the severity of outcomes. More inclusive research, regulatory policies, and tailored risk assessments are needed to address such inequities and reduce exposure.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 344-354"},"PeriodicalIF":2.9,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of polyunsaturated fatty acids in neurodevelopmental pediatric outcomes in the settings of gestational diabetes and obesity: A comprehensive review","authors":"Urja Ashish Mhatre ,&nbsp;Ishika Jindal ,&nbsp;Arina Mojavery ,&nbsp;Bianca-Marie Thompson ,&nbsp;Samar Salah Karar ,&nbsp;Mariana Rubio Aparicio ,&nbsp;Nadine Simon Abusada ,&nbsp;Livas Kwarisiima ,&nbsp;Amar Basil Ghadieh ,&nbsp;Hossam Tharwat Ali","doi":"10.1016/j.neuroscience.2025.06.019","DOIUrl":"10.1016/j.neuroscience.2025.06.019","url":null,"abstract":"<div><div>Obesity is one of the major concerns of global health. Globally, 6–12% of women with obesity also curse with gestational diabetes mellitus (GDM). Obesity and GDM constitute a major risk to maternal and fetal health with evidence suggesting an association with offspring cardiometabolic risk, respiratory disorders, and neurodevelopmental problems. Fatty acids, specifically polyunsaturated fatty acids (PUFAs), play a crucial role in fetal neurodevelopment and during early life stages. In addition to their neurogenesis-promoting properties, PUFAs have anti-apoptotic effects and provide neuroprotection against brain injury and oxidative stress. Some lipid metabolism enzymes have been recognized at synaptic terminals, proving PUFAs play a role in synaptogenesis, locally modulating synaptic transmission. On a cellular level, PUFAs suppress the production of arachidonic-acid-derived eicosanoids which modulate the production of pro-inflammatory and immunoregulatory cytokines. On a subcellular level, when ingested through the diet, PUFAs are distributed and enriched into cells and their membranes where they impact both metabolism and survival. For instance, mitochondria maintain both cellular homeostasis and calcium concentrations in the cell. Maternal PUFA concentrations during pregnancy are hypothesized to be associated with children’s cognitive and neuropsychiatric outcomes, including intelligence and IQ traits and autism spectrum disorders. Most recent evidence demonstrated a positive association between maternal dietary intake of PUFAs and fetal neurodevelopment. Nevertheless, establishing clear, evidence-based guidelines on the appropriate types, doses, and timing of PUFA supplementation for high-risk pregnancies could improve maternal and pediatric health outcomes.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 227-238"},"PeriodicalIF":2.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}