Developmental Neuroscience最新文献

{"title":"Branched Chain Amino Acid Metabolism in Developmental Brain Injury: Putative Mechanisms and Therapeutic Potential.","authors":"Margaret M Cassidy, Marc Yudkoff, Rebecca C Ahrens-Nicklas, Ana G Cristancho","doi":"10.1159/000545099","DOIUrl":"10.1159/000545099","url":null,"abstract":"<p><strong>Background: </strong>Branched chain amino acid (BCAA) metabolism plays roles in various cellular processes, including energy homeostasis, anabolic signaling, and production of glutamate, the primary excitatory neurotransmitter. Emerging evidence also suggests BCAA metabolism has relationships to inflammatory and hypoxic cellular responses. Recent work in adult and adolescent clinical populations has suggested that BCAA dietary supplementation may improve outcomes associated with traumatic brain injury. Given these links, examining the putative mechanisms and potential therapeutic applications of modulating dietary BCAA content in the context of inflammatory and hypoxic developmental brain injury may reveal mechanisms for intervention in affected infants.</p><p><strong>Summary: </strong>Inflammatory and hypoxic brain injuries influence the dynamics of BCAA metabolism in the fetal brain. Inflammatory insults to the developing brain may increase BCAA catabolism downstream of the branched chain ketoacids (BCKAs). The effect of altered BCAA metabolism on the pathophysiology of inflammatory developmental brain injury is currently unclear but may play a role in microglial response. Hypoxic brain injury seems to increase BCAA concentration in the fetal brain, possibly because of re-amination of BCKAs to the parent BCAAs, or via increased protein breakdown during hypoxia.</p><p><strong>Key messages: </strong>The apparent relationship between aberrant BCAA metabolism and inflammation or hypoxia warrants consideration of BCAA supplementation or restriction as a strategy for attenuating developmental brain injury that is associated with these pathologic events. This approach could entail alterations of maternal diet during pregnancy or the feeding of infant formula that is fortified with or restricted in BCAA. These types of interventions have been safely and effectively employed in cases of inborn errors of BCAA metabolism, suggesting feasibility in infant populations. Both in vitro and preclinical work is necessary to elucidate how BCAA supplementation or restriction may affect the sequelae of inflammatory and hypoxic developmental brain injury.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"68-82"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12353667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Pilot Study on Dynamic Multimodal Neuromonitoring for Predicting Neurodevelopmental Outcomes in Neonatal Hypoxic-Ischemic Encephalopathy.","authors":"Srinivas Kota, Lynn Bitar, Pollieanna Sepulveda, Soheila Norasteh, Hanli Liu, Lina F Chalak","doi":"10.1159/000545599","DOIUrl":"10.1159/000545599","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Multimodal neuromonitoring at the bedside is essential for understanding the pathophysiological mechanisms of brain injury and neurodevelopmental outcomes associated with neonatal hypoxic-ischemic encephalopathy (HIE). While previous research has focused on single modality neuromonitoring biomarkers to predict neurodevelopmental impairment (NDI) at 2 years of age, there remains significant gap in exploring the potential of multimodal physiological signal biomarkers to improve predictive accuracy. This study aimed to evaluate multimodal quantitative neuromonitoring biomarkers within the first day of life to improve prediction of NDI.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This prospective cohort study enrolled newborns (≥36 weeks) diagnosed with HIE at Parkland Hospital in Dallas, TX. A Sarnat examination was performed to determine the severity of HIE within the first 6 h of life, and the Total Sarnat Score (TSS) was calculated. Newborns with moderate and severe HIE received therapeutic hypothermia (TH). Neuronal noninvasive biomarkers including electroencephalogram (EEG) delta power (DP, 0.5-4 Hz) and neurovascular coupling (NVC), calculated as wavelet coherence between amplitude-integrated EEG and cerebral tissue oxygen saturation (SctO&lt;sub&gt;2&lt;/sub&gt;), were measured. NDI was defined as death or a cognitive score &lt;85 on the Bayley Scales of Infant and Toddler Development. The predictive ability of individual biomarkers (TSS, DP, and NVC) and their combination for NDI was evaluated using receiver operating characteristic (ROC) curves, with the area under the ROC curve (AUC) indicating prediction accuracy. Additionally, a Net Reclassification Index (NRI) analysis was conducted to assess the predictive performance of the three baseline models (TSS, DP, and NVC).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Forty-six newborns with mild to severe HIE were enrolled and neuromonitoring was initiated at 12 ± 6 h of life. Death or NDI was diagnosed in 18 (6 mild, 10 moderate, 2 severe) infants. Eight out of 46 infants did not complete the 18-24 months follow-up but had a normal examination prior. The combination of all three biomarkers (TSS, DP, and NVC) yielded the highest AUC of 0.755 (95% CI: 0.569-0.941), with sensitivity of 0.750, specificity of 0.769, positive predictive value of 0.800, and negative predictive value of 0.714, outperforming individual biomarkers or two-marker combinations. Furthermore, the NRI analysis demonstrated that the combined model achieved the highest NRI value (0.5577), indicating the strongest improvement in risk classification.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;This study emphasizes the importance of implementing multimodal neuromonitoring and integrating quantitative biomarkers at the bedside during the first day of life to provide objective metrics on brain health in addition to neurological exam. These approaches demonstrate potential for enhancing the prediction of encephalopathy severity, brain injury, an","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"85-96"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12353051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune Synaptopathy and Sex Differences in Recognition Memory from Neonatal <i>Staphylococcus epidermidis</i> Infection.","authors":"Wing Ki Chan, Seyedeh Marziyeh Jabbari Shiadeh, Janne Lenzig, Pernilla Svedin, Sofia Rasmusson, Oceane Vigne, Vanessa Veit, Tetyana Chumak, Maryam Ardalan, Carina Mallard","doi":"10.1159/000548381","DOIUrl":"10.1159/000548381","url":null,"abstract":"<p><strong>Introduction: </strong>Staphylococcus epidermidis (SE) is a predominant hospital-acquired bacterium leading to late-onset sepsis in preterm infants. Recent findings have suggested that postnatal SE infection is associated with short-term neurodevelopmental consequences. However, the potential effects of postnatal SE infection on long-term neuronal plasticity and cognitive functions, which are sensitive to early life brain insults, remain unclear. In light of these findings, we investigated the effects of postnatal SE infection on recognition memory function using a neonatal mouse model.</p><p><strong>Methods: </strong>On postnatal day 4, male and female C57Bl/6 mice were injected intraperitoneally with either 3.5 × 107 colony-forming units of SE or sterile saline. On postnatal day 45 (±5 days), the mice were subjected to the novel object recognition test (NORT) to assess recognition memory function. Following NORT, the brains of the mice were collected for neuronal plasticity analyses by considering maturation of neurons and 3-D analysis of synaptic plasticity and hippocampal, measuring the nerve growth factor (NGF) expression.</p><p><strong>Results: </strong>Postnatal SE infection induced long-term, sex-specific effects on recognition memory and hippocampal neuroplasticity. Female SE-infected mice showed enhanced recognition memory, whereas males showed no significant difference in the recognition memory after neonatal SE infection. At the cellular level, both sexes displayed a significant decrease in doublecortin-positive neurons in the dentate gyrus after SE infection, indicating impaired neuroplasticity. However, male mice showed increased spine density, particularly of immature thin spines and disrupted spatial organization of spines, while females demonstrated no change in spines. Notably, SE infection elevated hippocampal NGF expression in males, but not in females, suggesting sex-specific molecular responses that may contribute to the observed differences in neuroplasticity and cognitive outcomes.</p><p><strong>Conclusion: </strong>This study demonstrates that postnatal SE infection induces long-lasting, sex-specific changes in recognition memory. Early life immune activation disrupted hippocampal neuroplasticity, with males showing greater vulnerability. These findings indicate distinct neurodevelopmental trajectories shaped by neonatal immune challenges in preterm infants, with implications for understanding sex-specific cognitive outcomes.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"337-361"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034625","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":"Androgen Aggravates Chorioamnionitis-Induced White Matter Brain Injury and Neurobehavioral Impairments in Males.","authors":"Seline Vancolen, Mathilde Chevin, Marie-Julie Allard, Nour Bouzidi, Bernard Robaire, Guillaume Sébire","doi":"10.1159/000545074","DOIUrl":"10.1159/000545074","url":null,"abstract":"<p><p><p>Introduction: Group B Streptococcus (GBS) colonization leads to placental infection and inflammation, known as chorioamnionitis (CA). Fetal exposure to CA is linked to elevated risks of neurobehavioral impairments in offspring, including autism spectrum disorder, which is more prominent in males than females. In our preclinical model of GBS-induced CA, males exhibited heightened placental inflammation compared to females, correlating with more severe subsequent neurobehavioral impairments. We hypothesize that androgens upregulate the placental immune response in male fetuses, potentially contributing to GBS-induced autistic-like traits in male offspring. Our previous findings demonstrated that there were reduced pro-inflammatory cytokines and polymorphonuclear cell infiltration in flutamide (androgen receptor antagonist) plus GBS-infected compared to vehicle plus GBS-infected placenta. In this study, we investigated the effect of end gestational androgen blockade on brain injury patterns and neurobehavioral outcomes in offspring in utero exposed to GBS CA.</p><p><strong>Methods: </strong>Lewis dams received daily injections of vehicle or flutamide from gestational day (G) 18-21, followed by saline or inactivated GBS injections from G19 to 21. Behavioral assessments were conducted from postnatal day (P) 9-40 and brains were dissected on P50.</p><p><strong>Results: </strong>Behavioral assessments revealed impaired social interactions in CA-exposed versus unexposed male rats. These impairments were not observed in flutamide-treated rats. Histological analysis of forebrains at P50 showed lateral forebrain ventricle enlargement and reduced periventricular white matter thickness, namely the corpus callosum and external capsule in offspring exposed to CA contrasting with an improvement in these outcomes observed in flutamide treated rats. Exposure to CA reduced the density of CC-1+ oligodendrocytes in the external capsule whereas flutamide mitigated this reduction in offspring at P50.</p><p><strong>Conclusion: </strong>These findings suggest a significant role for androgens in the skewed sex ratio observed in developmental impairments resulting from perinatal inflammation, underscoring the need for personalized sex-specific neuroprotective therapies. </p>.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"1-11"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12088651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Light Exposure duration on Severity and Long-Term Neurodevelopment following Photothrombotic Stroke in a Neonate.","authors":"Arya Jithoo, Tayla R Penny, Shu Wen Wen, Althea R Suthya, Yen Pham, Amy E Sutherland, Connie H Y Wong, Suzanne L Miller, Courtney A McDonald","doi":"10.1159/000544994","DOIUrl":"10.1159/000544994","url":null,"abstract":"<p><strong>Introduction: </strong>Perinatal stroke causes lasting neurological deficits and there are currently no effective treatment options. Established animal models of perinatal stroke do not always mimic the clinical presentation of neonatal injury or are technically challenging to perform. The photothrombotic (PT) stroke model is a minimally invasive method that replicates focal ischaemic injury. Few studies have applied the PT model in neonatal contexts, and none have examined both short- and long-term effects across varying injury severities. This study aimed to optimize a protocol to create a mild model of perinatal stroke and subsequently characterize injury progression, neuropathological impact, and motor deficits over time.</p><p><strong>Methods: </strong>On postnatal day 10 we used the PT method to induce perinatal stroke in rat pups. Pups were exposed to various light exposure times (10, 20, or 30 min) to determine the optimal time needed to produce a mild and reproducible cortical stroke injury. Behavioural assessments were conducted on days 4, 10, 20, and 30 post-injury. Brains were collected for analysis on days 3 and 40 post-injury.</p><p><strong>Results: </strong>Three days post-injury, the 20 and 30 min group had significant focal lesions and microbleeds were present in each of the PT groups. All PT groups showed significant neuron loss in the peri-infarct region and the thalamus, and microglia activation in multiple brain regions. As 30 min of light exposure showed extensive cortical tissue loss (>70%), we excluded the 30-min group from long-term assessment. 40 days post-injury, the 10 and 20 min groups demonstrated significant tissue loss and neuronal loss in the peri-infarct region and thalamus, but only the 20 min group showed neuron loss in the hippocampus. The 10 and 20 min groups both demonstrated ongoing motor deficits.</p><p><strong>Conclusion: </strong>Our results demonstrate that increasing light exposure time in PT stroke results in a more severe stroke phenotype. 30 min of light exposure resulted in a severe injury at only 3 days post insult, therefore, was not further investigated. 10 and 20 min of light exposure had a similar effect at 3 days, however, after 40 days the 20 min exposure time created a moderate injury phenotype. From this study, we propose that 10 min of light exposure is optimal to create a mild stroke phenotype and is associated with motor deficits and altered neuropathology. This injury phenotype provides a focal and reproducible insult, while still being mild enough to feasibly test therapeutics.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"30-49"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558714","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":"Auditory Deficits in a Mouse Model of First-Trimester Prenatal Alcohol Exposure.","authors":"Mark Jessup, Abigail L Tice, Addison McNeill, Avery Tangen, Maya L Liu, Deirdre M McCarthy, Pradeep G Bhide, Jennifer L Steiner, Yuan Wang","doi":"10.1159/000545065","DOIUrl":"10.1159/000545065","url":null,"abstract":"<p><strong>Introduction: </strong>Prenatal alcohol exposure (PAE) can lead to a wide spectrum of deficits in growth and neurological function, and there is an established link between PAE and auditory dysfunction. However, the effects of PAE on auditory development are complex and vary depending on the age and pattern of alcohol exposure.</p><p><strong>Methods: </strong>In this study, we developed a mouse model of PAE during the first half of the gestational period, mimicking alcohol consumption during the first trimester of pregnancy in humans.</p><p><strong>Results: </strong>This exposure did not affect overall growth or induce anxiety-related symptoms in the offspring, as indicated by normal body weight change and largely unchanged behaviors in the open field and elevated zero maze tests. However, several aspects of auditory function were affected by PAE. Offspring born from prenatal alcohol-exposed dams displayed smaller auditory brainstem responses (ABRs) at 2-month-old as compared to those from control dams, suggesting weakened neuron synchronization within auditory brainstem circuits. Additionally, a reduction in the reproducibility of ABR peaks III/IV was observed in PAE offspring. In contrast, the overall hearing sensitivity and neuron transmission was not affected by PAE, as evaluated by ABR thresholds or peak latencies. In an acoustic startle test, PAE offspring failed to display prepulse inhibition to low levels of prepulses more frequently than control offspring at both 2 weeks old and 2 months old, suggesting an early-onset and lasting deficit in auditory gating or sound level differentiation.</p><p><strong>Conclusion: </strong>These results demonstrate that mice exposed to alcohol during early gestation have largely preserved auditory responses but show significant alterations in specific features of auditory processing.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"12-29"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607044","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":"Neocortex Folding in Primates up to Human: Evolution and Mechanisms.","authors":"Katherine R Long, Wieland B Huttner, Takashi Namba","doi":"10.1159/000547228","DOIUrl":"10.1159/000547228","url":null,"abstract":"<p><strong>Background: </strong>Folding of the neocortex is a fundamental feature of brain development in many mammalian species, notably in most non-human primates and in particular in human. Cortical folding is thought to allow a larger cortical surface area, with a greater number of neurons, to fit into the limited size of the cranial cavity.</p><p><strong>Summary: </strong>Here, we review the following key topics related to cortical folding. We first discuss the principles of cortical folding and dissect the factors contributing to the mechanical asymmetry that is thought to have a key role in driving fold formation. We then address the evolution of cortical folding and discuss the two principal types of folding, conserved and evolved, and the roles of neuron production vs. neuron migration in these. We also review the different model systems used, such as human tissue/cell-based, animal, and computational models of cortical folding.</p><p><strong>Key messages: </strong>This includes a discussion of human malformations of cortical folding, the potential of cerebral organoids to study folding, the power of the ferret model to dissect mechanisms of cortical folding, and the use of computational models to make predictions about cortical folding. Finally, we address future perspectives of folding research and outline directions that research may take.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"314-324"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144592853","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 Bioinformatic Investigation into a Unique Human FOXM1 Exon Variant and Its Relevance to Gyrencephaly.","authors":"Mikaela Barresi, Alice Johnstone, Mary Tolcos","doi":"10.1159/000545713","DOIUrl":"10.1159/000545713","url":null,"abstract":"<p><strong>Introduction: </strong>Gyrification is a shared phenotype of brain development across many species. The identification of human- and primate-specific genes is a topic of great research interest to uncover the genetic mechanisms that drive human gyrification. Here we investigated a human transcript variant of FOXM1 with a unique ninth exon proposed to have a crucial role in primate gyrification.</p><p><strong>Method: </strong>We performed comprehensive bioinformatic analyses, including several BLASTs and multiple sequence alignment, utilising available deposited sequencing data. We aimed to determine the degree of conservation of human FOXM1 exon 9 across a wide range of species, with a particular focus on gyrencephalic primates. Furthermore, we aimed to determine the degree of conservation of the remaining regions of FOXM1 across a subset of gyrencephalic and lissencephalic species.</p><p><strong>Results: </strong>Our results revealed that the exon is only partially detected in four other primates, challenging its presumed conservation in humans, apes, and other primates. The remaining regions of FOXM1 had a remarkably high level of conservation, and, given its role in regulating proliferation and differentiation, the results suggested that FOXM1 may be required for early brain development across all species. However, the sporadic presence of the exon 9 sequence even in other gyrencephalic primates raises questions about its indispensability in the process of gyrification.</p><p><strong>Conclusion: </strong>Therefore, we conclude that the FOXM1 transcript variant comprising the exon 9 sequence in its entirety could be more appropriately reclassified as a human-specific cortical folding variant not found in other species. This research lays the foundation for further investigating the role of FOXM1 exon 9 in human gyrification and brain development.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"155-163"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144058917","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":"Aquaporins: Bridging Normal Brain Development and Neurodevelopmental Disorder Mechanisms.","authors":"Fateme Azizi, Wing Ki Chan, Maryam Ardalan","doi":"10.1159/000545512","DOIUrl":"10.1159/000545512","url":null,"abstract":"<p><strong>Background: </strong>Homeostasis of water content in the brain during fetal development is of crucial physiological importance. Aquaporins (AQPs) play a critical role in maintaining brain water balance, supporting normal brain development, and are increasingly recognized for their relevance in understanding neurodevelopmental disorders.</p><p><strong>Summary: </strong>This review provides a comprehensive overview of AQPs and their essential roles in the central nervous system (CNS), specifically AQP4, AQP11, and AQP9, which play a crucial role in water transport in the brain, maintaining water homeostasis and facilitating water movement across cell membranes. The review also highlights how disruptions in AQP expression and function may contribute to the pathology of neurodevelopmental disorders such as autism and Fragile X syndrome.</p><p><strong>Key messages: </strong>AQPs are vital for brain water regulation and normal neural development. Altered expression or function of AQPs can impact blood-brain barrier integrity, neuroinflammation, and synaptic activity. AQP dysfunctions are linked to neurodevelopmental disorders and may represent promising therapeutic targets.</p>","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"115-129"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143732834","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":"Erratum.","authors":"","doi":"10.1159/000549838","DOIUrl":"10.1159/000549838","url":null,"abstract":"&lt;p&gt;&lt;p&gt;In the article \"Caffeine as a Treatment for Perinatal Hypoxic-Ischemic Brain Injury: The Potential Risks and Benefits\" [Dev Neurosci. 2025; Online ahead of print. https://doi.org/10.1159/000545126] by Zhou et al., the authors noted that there were several errors within their article. The corrections are listed below.In the section \"Adenosine and Adenosine Receptors\" currently reads, \"By contrast, A2 adenosine receptor knockout mice that were subjected to common carotid ligation and hypoxia at P7 had more severe brain injury with worse performance in motor behavioural tests, compared with wild-type mice [30].\" Should correctly read, \"By contrast, A2A adenosine receptor knockout mice that were subjected to common carotid ligation and hypoxia at P7 had more severe brain injury with worse performance in motor behavioural tests, compared with wild-type mice [30].\"Reference 47 was erroneously included and is not an intended citation, this reference should be deleted. Under the subheading, \"Caffeine: Perspectives and Future Directions\", the following sentences should correctly read:It is unclear why studies in rodents suggest benefit with prophylactic caffeine, before HI, whereas limited benefit with prophylactic caffeine in lambs [39], and deleterious effects of adenosine A1 receptor blockade [20]. Speculatively, this difference may reflect that these rodent studies used inhalational hypoxia and so caffeine may help avoid apnea [48] and so reduce the risk of deep hypoxemia. Regardless of the precise mechanism, these findings strongly suggest that considerable caution is needed before considering human studies.The following two errors table 1 should be corrected. For the study Yang et al., 2022, under key findings was missing before \"Microglia M2 polarisation\". For the study, Sabir et al., 2023 and in row 8 the study year was corrected to 2023.The corrected table is shown below:Table 1.Summary of preclinical studies on the effects of caffeine for perinatal hypoxic-ischemic brain injuryStudySpecies and ageN per groupInsultDose and timingKey findingsDi Martino et al. [34] (2020)P10 micen = 8-10Common carotid artery ligation and hypoxia (1 h)Caffeine 5 mg/kg, i.p. immediately after HI↓ Grey and white matter lesion size↓ Amoeboid microglia and apoptotic cellsn = 6-8Caffeine started at 6, 12 or 24 h after HINo neuroprotective effectWinerdal et al. [35] (2017)P10 micen = 13-29Common carotid artery ligation and hypoxia (1 h)Caffeine 5 mg/kg i.p. immediately after HI↓ Brain atrophy↑ Time on the rotorod behavioral testPotter et al. [37] (2018)P6 ratsn = 6Common carotid artery ligation and hypoxia (2 h)Caffeine citrate 20 mg/kg i.p. administration immediately after HI↑ Performance in rotarod and water maze behavioral tests↑ Silent gap detection (speech detection)Bernis et al. [38] (2025)P7 ratsn = 5-50Common carotid artery ligation and hypoxia (90 min)Caffeine citrate 15, 20 or 40 mg/kg i.p. administration immediately before HI or 40 mg/kg immediately after","PeriodicalId":50585,"journal":{"name":"Developmental Neuroscience","volume":" ","pages":"164-166"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145991605","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}