IBRO Neuroscience Reports最新文献

{"title":"Tracing the threads: How toxic metals contribute to neurodegeneration","authors":"Elyse Wiebe ,&nbsp;Zaccheaus Olayiwola ,&nbsp;Olamide Adebiyi","doi":"10.1016/j.ibneur.2025.12.008","DOIUrl":"10.1016/j.ibneur.2025.12.008","url":null,"abstract":"<div><div>Brain disorders affect more than one in three people globally, representing a leading cause of disability and morbidity. While the etiology of several of these disorders remains elusive, it is increasingly evident that both genetic and environmental factors contribute to their onset and progression. Given the persistent effects of environmental exposures on biological systems, this review highlights the role of heavy metals (particularly lead, mercury, vanadium, and chromium) in altering behaviour and contributing to the development of neurodegenerative and demyelinating diseases, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. We discuss the sources of human and animal exposure to these metals, focusing on the underlying mechanisms by which they promote neurotoxicity, including oxidative stress, mitochondrial dysfunction, protein aggregation, and disruption of the blood–brain barrier. Additionally, we explore how exposure affects genetic and epigenetic interactions and provide epidemiological data linking metal toxicity to brain disorders. By exploring evidence from animal models and human epidemiological studies, with public health relevance, we extend our discussion beyond descriptive neurotoxicology to highlight exposure to these metals as a unifying upstream driver of various brain disorders. Finally, considering gaps in current knowledge, particularly regarding the impact of transgenerational exposures, we propose directions for future research. These insights not only enhance our understanding of metal-induced neurodegeneration but also underscore the need for targeted public health interventions and policies to reduce exposure, especially in vulnerable populations and communities.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 34-48"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145838510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared genetic architecture of psychiatric disorders and ocular diseases: Evidence from genome-wide analyses","authors":"Zhao-yang Zhang ,&nbsp;Huan-xi Liu ,&nbsp;Xiao-jia Ma ,&nbsp;Ting-ting Wang ,&nbsp;Xiang-wen Wang ,&nbsp;Wei-jian Han ,&nbsp;Cong Zhou ,&nbsp;Jun-jie Luan ,&nbsp;Ping Sun","doi":"10.1016/j.ibneur.2026.02.003","DOIUrl":"10.1016/j.ibneur.2026.02.003","url":null,"abstract":"<div><h3>Objective</h3><div>Psychiatric disorders are frequently comorbid with ocular diseases, yet the shared genetic basis and potential causal links remain unclear. This study aimed to systematically investigate the shared genetic architecture, bidirectional causality, and implicated biological pathways between common psychiatric disorders and ocular diseases.</div></div><div><h3>Methods</h3><div>We analyzed four psychiatric disorders and eight ocular diseases using an integrative genome-wide analytical framework. We used linkage disequilibrium score regression (LDSC) to estimate genome-wide genetic correlations and local genetic correlation analysis (LAVA) to identify region-specific shared signals. Bidirectional Mendelian randomization (MR) was performed to assess causal relationships. Shared loci were identified using conditional/conjunctive false discovery rate (cond/conjFDR) and evaluated by colocalization. Variants were then annotated and mapped to genes using FUMA, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and protein–protein interaction (PPI) network analyses to prioritize pathways and hub genes.</div></div><div><h3>Results</h3><div>LDSC revealed significant genetic correlations between anxiety disorder and conjunctivitis, and between major depressive disorder (MDD) and several ocular diseases, including cataract, conjunctivitis, and keratitis. LAVA further confirmed shared, directionally consistent local genetic effects between MDD and these ocular phenotypes across multiple genomic regions. Bidirectional MR suggested that MDD increases the risk of cataract, conjunctivitis, and keratitis, with evidence for bidirectional causality between cataract and MDD. The conjFDR analysis (conjFDR &lt; 0.05) identified approximately 70 independent shared loci (lead SNPs). Functional annotation prioritized representative SNPs with potential functional and regulatory evidence, including rs1029871 and rs678 for bipolar disorder–cataract, rs1042602 for MDD–cataract, and rs12185233 and rs17651549 shared between schizophrenia and both cataract and conjunctivitis. Enrichment analyses of mapped genes suggested that pathways related to hyaluronic acid and amino acid metabolism, cholinergic signaling, and immune–inflammatory processes may contribute to the comorbidity between psychiatric and ocular diseases.</div></div><div><h3>Conclusion</h3><div>This genome-wide study reveals genetic links between psychiatric and ocular diseases and provides evidence for bidirectional causality in selected phenotypes. Metabolism–inflammation–related pathways may contribute to comorbidity along the eye–brain axis, offering leads for future mechanistic validation.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 232-243"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep deprivation and memory: A neurobiological perspective","authors":"Kehinde O. Adeniji BSc, MSc ,&nbsp;Olumayowa O. Igado DVM, MSc, PhD ,&nbsp;Funmilayo E. Olopade MBBS, MPH, MSc, PhD ,&nbsp;Omowumi M. Femi-Akinlosotu BDS, MSc, PhD","doi":"10.1016/j.ibneur.2026.01.010","DOIUrl":"10.1016/j.ibneur.2026.01.010","url":null,"abstract":"<div><div>Memory consolidation and the preservation of cognitive function are fundamentally influenced by sleep. Lack of sleep affects synaptic plasticity and neurogenesis, as well as oxidative stress and neuroinflammation, all of which impair memory accuracy, cognitive flexibility, and attention. The behavioural repercussions include decreased learning ability, attentional problems, emotional dysregulation, and heightened vulnerability to false memories. This review examines the neurobiological impact of sleep deprivation on memory and cognition, emphasising how the brain systems performing these functions are disrupted by insufficient sleep. The distinct sleep stages that are in support of declarative, procedural, and emotional memory, drawing on contemporary concepts such as the synaptic homeostasis hypothesis and the active system consolidation theory, were emphasised. We highlighted how sleep deprivation can affect important areas, especially the hippocampus, and cause problems with neurotransmitter systems and immune regulation. Preventative and therapeutic approaches, such as pharmacological supports, behavioural interventions, and the cognitive advantages of recovery sleep and naps, were also enumerated. These insights on how sleep and memory interact are vital for enhancing learning outcomes, mental health, and long-term brain resilience.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 170-180"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical exercise as a non-pharmacological strategy to enhance glymphatic function","authors":"Arman Ghayourvahdat ,&nbsp;Hannaneh Azimizonuzi ,&nbsp;Moslem Ahmed","doi":"10.1016/j.ibneur.2026.01.014","DOIUrl":"10.1016/j.ibneur.2026.01.014","url":null,"abstract":"<div><div>The glymphatic system plays a critical role in clearing metabolic waste and neurotoxic proteins from the brain, and its dysfunction is implicated in neurodegenerative diseases such as Alzheimer’s disease (AD). Emerging evidence indicates that physical exercise enhances glymphatic function through multiple mechanisms, including increased cerebrospinal fluid (CSF) influx, improved perivascular clearance, astrocytic aquaporin-4 (AQP4) polarization, and modulation of vascular and sleep-dependent processes. Preclinical studies demonstrated that voluntary wheel running and aerobic exercise reduce amyloid-β (Aβ) accumulation, attenuate neuroinflammation, and improve cognitive performance in both aging and AD mouse models, with benefits being highly dependent on AQP4 expression and the timing of intervention. Translational evidence in humans showed that structured aerobic and multicomponent exercise increases glymphatic and meningeal lymphatic activity, enhances vascular dynamics, reduces systemic inflammation, and improves sleep quality, leading to measurable cognitive gains. Despite these promising findings, methodological challenges—such as limitations of non-invasive imaging, difficulty establishing causality, and reliance on short-term interventions—highlight the need for longitudinal, multimodal studies that integrate imaging, cardiovascular, sleep, and cognitive metrics. Collectively, these data suggest that exercise represents a potent non-pharmacological strategy to augment glymphatic clearance, preserve neural homeostasis, and reduce the risk of cognitive decline. This review will summarize evidence on exercise-induced glymphatic enhancement, highlight mechanisms, and identify research gaps for future studies on brain health.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 206-217"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146165244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the impact of intracerebroventricular norepinephrine on spatial memory in rats: Insights into sporadic Alzheimer’s pathogenesis","authors":"Mohammad Amir Sharifi Moien,&nbsp;Seyed Javad Saghravanian,&nbsp;Masoud Fereidoni","doi":"10.1016/j.ibneur.2025.12.012","DOIUrl":"10.1016/j.ibneur.2025.12.012","url":null,"abstract":"<div><div>One consequence of stress is the increased release of norepinephrine (NE) in the central nervous system, primarily driven by activation of the sympathetic nervous system. Given the importance of chronic stress in the development and progression of Alzheimer’s disease (AD), clarifying the specific contributions of stress-related pathways, including the sympathetic axis and the hypothalamic-pituitary-adrenal (HPA) axis, is critical. In this study, we examined the effects of repeated central NE administration, as a potential contributor to stress-related cognitive impairment, on spatial memory in rats, alone or in combination with a low-dose streptozotocin (STZ) model of sporadic AD. Forty-nine rats were assigned to seven groups: control (no treatment), sham (saline; i.c.v.), low-dose streptozotocin (0.5 mg/kg, i.c.v.), norepinephrine administration at either 1 (adolescent) or 3 (adult) months of age (30 or 50 μg, respectively; i.c.v.), and co-administration of norepinephrine with streptozotocin at 1 or 3 months of age. Spatial memory was assessed using the Morris Water Maze test. Norepinephrine administration during adolescence and adulthood impaired spatial memory similar to streptozotocin in different parameters of the MWM, with adult rats showing the most significant vulnerability (p &lt; 0.001). However, co-administration of both substances did not exacerbate the impairment caused by each alone. The results suggest that norepinephrine may impair cognition through mechanisms distinct from those of STZ-induced deficits. Additionally, they raise questions about the contribution of the sympathetic axis of chronic stress to the progression of sporadic AD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 84-93"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145921807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum trimethylamine N-oxide (TMAO) and trimethyllysine in patients with amyotrophic lateral sclerosis (ALS): An exploratory case–control study","authors":"Salvatore Sotgia ,&nbsp;Angelo Zinellu ,&nbsp;Stefano Zoroddu ,&nbsp;Maria Ida Pateri ,&nbsp;Eleonora Loi ,&nbsp;Andrea Pisano ,&nbsp;Angela Sabalic ,&nbsp;Davide Tutedde ,&nbsp;Ana Florencia Vega-Benedetti ,&nbsp;Francesca Floris ,&nbsp;Monica Puligheddu ,&nbsp;Paolo Valera ,&nbsp;Patrizia Zavattari ,&nbsp;Giuseppe Borghero ,&nbsp;Roberto Madeddu","doi":"10.1016/j.ibneur.2026.02.006","DOIUrl":"10.1016/j.ibneur.2026.02.006","url":null,"abstract":"<div><div>Trimethylamine N-oxide (TMAO) is a gut microbiota–derived metabolite implicated in protein homeostasis, inflammation, and chronic disease, but its relevance in amyotrophic lateral sclerosis (ALS) remains poorly characterized. In this exploratory pilot study, we quantified circulating TMAO and related trimethylammonium-containing compounds in a Sardinian ALS cohort using targeted LC–MS/MS. Serum samples were collected under fasting conditions from 12 ALS patients and 8 age- and sex-matched healthy controls. Median serum TMAO levels were markedly higher in ALS patients than in controls (27.9 vs. 4.0 µmol/L, P &lt; 0.05), with substantial inter-individual variability in the ALS group (range 2.4–125.0 µmol/L). Trimethyllysine (TML) concentrations were also significantly elevated in ALS (0.43 vs. 0.34 µmol/L, P &lt; 0.05), whereas choline, carnitine, betaine, ergothioneine, and γ-butyrobetaine levels did not differ between groups. Most ALS patients were receiving acetyl-<span>L</span>-carnitine (ALCAR) supplementation, suggesting that ALCAR intake may contribute to the observed metabolite profiles. Overall, these findings indicate alterations in trimethylammonium-containing compound metabolism in ALS and underscore the need for larger, well-controlled studies to determine whether such changes reflect disease-related mechanisms, treatment effects, or their interaction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 227-231"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-time autonomic responses to insulin-induced hypoglycaemia in volunteers with type I diabetes compared to controls","authors":"Maria Bitsch Poulsen ,&nbsp;Christina Brock ,&nbsp;Peter Oketa-Onyut Julu","doi":"10.1016/j.ibneur.2025.12.014","DOIUrl":"10.1016/j.ibneur.2025.12.014","url":null,"abstract":"<div><h3>Objective</h3><div>Hypoglycaemia is a severe risk of insulin-treatment in diabetes, and in type 1 diabetes (T1D), the normal counterregulatory autonomic mechanisms are diminished. This study investigated the recovery of both parasympathetic and sympathetic tone from hypoglycaemia to normoglycemia in T1D in comparison to controls.</div></div><div><h3>Methods</h3><div>Six individuals with T1D without complications and six age and sex-matched controls were included in this explorative acute intervention study. Electrocardiogram, skin blood flow (SBF, sympathetic measure), cardiac vagal tone (CVT, parasympathetic measure), and plasma glucose were measured at baseline, at hypoglycaemia, and at 30-, 60-, 120-, and 240-minutes post-hypoglycaemia.</div></div><div><h3>Results</h3><div>Insulin injection induced hypoglycaemia with a reduction of CVT in both controls and individuals with T1D, but no consistent response in SBF. Normoglycemia was reached by 120-minutes, though T1D showed delayed glucose recovery at 30- and 60-minutes with an overshoot at 240-minutes. SBF showed no consistent changes but was lower in T1D at 240-minutes. CVT increased consistently, recovering after 60-minutes in the individuals with T1D and 30-minutes in the controls, with a heightened at 240-minutes in the individuals with T1D.</div></div><div><h3>Conclusion</h3><div>CVT as a measure of cardiac parasympathetic function responds consistently to both hypoglycaemia and during recovery in individuals with T1D and controls, but SBF as a measure of cutaneous sympathetic function does not. There are defective counterregulatory mechanisms in T1D shown by delayed recovery of blood glucose and rebound overactivity of both cardiac parasympathetic tone and sympathetic cutaneous vasoconstriction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 119-124"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic effectiveness of conditioned medium derived from adipose tissue mesenchymal stem cells and dehydroepiandrosterone in a rat model of spinal cord injury","authors":"Farrokh Modarresi ,&nbsp;Gholam Reza Kaka ,&nbsp;Mehdi Raei ,&nbsp;Fatemeh Rezaei-Tazangi","doi":"10.1016/j.ibneur.2025.12.010","DOIUrl":"10.1016/j.ibneur.2025.12.010","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background and objective&lt;/h3&gt;&lt;div&gt;Spinal cord injury (SCI) is a severe neurological disorder that leads to significant complications, including loss of bladder/bowel control and increased infection risk. The current standard treatment involves methylprednisolone administration and surgical decompression, but finding an effective therapy with minimal side effects remains a major challenge. This study aimed to investigate the effects of an optimized conditioned medium derived from rat adipose-derived mesenchymal stem cells (AD-MSCs) and dihydroepiandrosterone (DHEA) on behavioral indices, oxidative stress, stereological parameters, and histopathological outcomes in rats with compressive spinal cord injury (SCI).&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Material and methods&lt;/h3&gt;&lt;div&gt;In this study, 60 adult female rats were randomly divided into five groups: Sham group (laminectomy + intraperitoneal injection of 1 % dimethyl sulfoxide [DMSO], 200 µL for seven consecutive days), SCI-induced group (SCI induction + intraperitoneal injection of 1 % DMSO, 200 µL for seven consecutive days), Treatment group 1 (SCI induction + intraperitoneal injection of DHEA [30 mg/kg] dissolved in 1 % DMSO for seven consecutive days), Treatment group 2 (SCI induction + intraperitoneal injection of conditioned medium [200 µL] for seven consecutive days), Treatment group 3 (SCI induction + intraperitoneal injection of DHEA [30 mg/kg] dissolved in 1 % DMSO followed by conditioned medium [200 µL] for seven consecutive days). Behavioral assessments were performed using the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and the rotarod test. Additionally, the levels of antioxidant enzymes—catalase, glutathione (GSH), superoxide dismutase (SOD), and the lipid peroxidation marker malondialdehyde (MDA)—were measured using respective assay kits. For stereological evaluation (to estimate neuronal and non-neuronal cell counts, gray and white matter volumes, spinal cord volume, and lesion area) and histopathological assessment (to evaluate inflammation, necrosis, and hemorrhage indices), tissue samples were stained with Cresyl Violet.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The findings revealed that in the SCI-induced group, motor function, neuronal cell number in spinal gray matter, non-neuronal cell number in the spinal cord, white and gray matter volumes, total spinal cord volume, and levels of catalase, GSH, and SOD were significantly reduced compared to the sham group. Conversely, the spinal lesion volume and MDA levels were elevated. Treatment with DHEA, AD-MSC-conditioned medium, or their combination reversed these effects. Notably, the combined treatment group exhibited more pronounced therapeutic improvements compared to monotherapy groups.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;The administration of DHEA and AD-MSC-conditioned medium, particularly in combination, appears to enhance motor function, elevate antioxidant enzyme activity, reduce lipid peroxidation, improve spinal","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 264-275"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prefrontal TDCS does not improve working memory performance in individuals with chronic alcohol and tobacco use","authors":"Franziska Göttgens ,&nbsp;Ute Habel ,&nbsp;Paul Wallheinke ,&nbsp;Julie A. Blendy ,&nbsp;Carmen Weidler","doi":"10.1016/j.ibneur.2026.01.011","DOIUrl":"10.1016/j.ibneur.2026.01.011","url":null,"abstract":"<div><div>Working memory (WM) deficits are common in psychiatric disorders that are associated with decreased prefrontal cortex activity. As WM is essential for cognitive functions, deficits interfere with daily life and treatment. The lateralization of WM components remains unclear, but stimuli matching, often assessed using the n-back task, has been associated with right-hemispheric dominance. This study examines whether anodal transcranial direct current stimulation (tDCS) targeting the right dorsolateral prefrontal cortex (DLPFC) could enhance WM performance in alcohol-dependent patients (AD), tobacco users (TU) and healthy controls (HC). In a double-blind, sham-controlled study, tDCS was applied to upregulate right DLPFC activity. A total of 46 participants received anodal tDCS with a current intensity of 1.5 mA for 20 min or sham stimulation. In addition to the 7x5cm anode, a large reference electrode (10x10cm) was situated over the contralateral supraorbital area. While being stimulated, participants performed the n-back task as a measure of WM performance. Results revealed no significant differences in WM performance between active and sham stimulated participants, nor between groups, and no significant interaction between stimulation condition and group. Bayesian analysis supported the null effects. These findings do not provide evidence that single-session right DLPFC stimulation reliably enhances working memory across all stimulus types. The outcomes may have been influenced by task–stimulation mismatch, sample heterogeneity, small sample size, and stimulation parameters, which could limit the ability to detect subtle tDCS effects in both clinical and healthy populations.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 196-205"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146074128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure to di(2-ethylhexyl) phthalate alters the association of glutamatergic proteins with PTEN in the hippocampus of male rat offspring","authors":"Natalia Kiknadze ,&nbsp;Elene Zhuravliova ,&nbsp;David Mikeladze","doi":"10.1016/j.ibneur.2025.12.005","DOIUrl":"10.1016/j.ibneur.2025.12.005","url":null,"abstract":"<div><div>Phthalates are extensively used chemicals known to have adverse effects on human health. Prenatal exposure to phthalates has been associated with potential disruptions in brain development and an elevated susceptibility to cognitive and behavioral disorders. The effects of phthalates on learning, memory, and related hippocampal processes have been widely studied; however, the molecular pathways through which phthalates modulate synaptic processes are not fully understood. Previous studies have shown that the molecular mechanism of DEHP-induced hippocampal neurotoxicity in the maturing male brain involves changes in phosphatase and tensin homolog (PTEN) subcellular location, which suppresses Akt/mTOR signaling and enhances GluN2B NMDA-mediated synapse depression. Immunoprecipitation experiments revealed that the prenatal administration of DEHP to rats led to a reduction in the association of the scaffold protein NHERF1, NMDA receptor subunits, AMPA receptor subunits, metabotropic glutamate receptor 5, and excitatory amino acid transporter-2 with PTEN in the hippocampus of offspring, while the overall quantity of these proteins remained unchanged. Furthermore, our results demonstrated that prenatal exposure of rats to phthalates resulted in downregulation of calcineurin phosphatase activity, decreased autophosphorylation of calcium/calmodulin-dependent protein kinase II, reduced protein kinase A activity, and upregulation of Akt kinase in the hippocampus of young rats. These findings suggest that the susceptibility of the PTEN protein interactome to phthalates in the glutamatergic postsynaptic density may influence synaptic plasticity at excitatory neurons in the hippocampus of offspring after exposure of parent rats to DEHP during gestation.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 25-33"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145789055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}