IBRO Neuroscience Reports最新文献

{"title":"Cardiovascular risk factors, aging, and incidence of dementia (CAIDE) risk score and its association with cognitive performance and volumetric brain measures in mild cognitive impairment","authors":"Yasaman Abtahi ,&nbsp;Marjan Falahati ,&nbsp;Sheyda Sharabiani ,&nbsp;Fatemeh Gila ,&nbsp;Saeed Omidi ,&nbsp;Farshad Goharmanesh ,&nbsp;Yousef Nourbakhsh ,&nbsp;Marziye Jalalian Chaleshtari ,&nbsp;Mohammad Hossein Nourbakhshi ,&nbsp;Parham Mahmoudi ,&nbsp;Raziyeh Zamiri ,&nbsp;Laya Dalir ,&nbsp;Zahra Gharehdaghi ,&nbsp;Hamide Nasiri ,&nbsp;Mahsa Mayeli ,&nbsp;Hannaneh Azimizonuzi ,&nbsp;for the Alzheimer’s Disease Neuroimaging Initiative","doi":"10.1016/j.ibneur.2025.12.007","DOIUrl":"10.1016/j.ibneur.2025.12.007","url":null,"abstract":"<div><h3>Background</h3><div>The Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) composite score is a promising measure connecting vascular health to cognitive decline; However, its association with brain imaging findings remains underexplored. This study aimed to evaluate the predictive value of the associations between CAIDE and structural brain measures in individuals with mild cognitive impairment (MCI).</div></div><div><h3>Methods</h3><div>Participants (n = 226) aged 55–90 years with available CAIDE scores and white matter hyperintensity (WMH) measurements and a diagnosis of amnestic MCI were included. Regression models were used to evaluate the association between CAIDE score and neuropsychiatric and imaging findings.</div></div><div><h3>Results</h3><div>Higher CAIDE scores were significantly correlated with lower MMSE scores (r = -0.22, p = 0.001) and higher CDR-SB (r = 0.34, p &lt; 0.001) and ADAS-Cog 11 scores (r = 0.38, p &lt; 0.001). CAIDE scores were significantly positively related to total cerebrum (β = 0.319), gray matter (β = 0.337), and hippocampal volumes (β = 0.250, all p &lt; 0.001). ROC analysis demonstrated that total gray matter (AUC = 0.70) and total brain (AUC = 0.69) were more accurate predictors of dementia risk compared to WMH volume (AUC = 0.52).</div></div><div><h3>Conclusion</h3><div>Higher CAIDE dementia risk scores were linked to poorer cognitive performance but showed limited association with WMH burden in individuals with MCI. Gray matter and hippocampal volumes were stronger correlates of dementia risk than WMH volume and CAIDE-related risk may be better captured by cortical and hippocampal structural changes rather than white matter disease.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 76-83"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145922387","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":"Frankincense improves motor symptoms and attenuates the progression of Paraquat (PQ)-induced Parkinson’s disease in mice by attenuating oxidative stress, inflammation, and apoptotic cell death and improving nerve growth factor gene expression","authors":"Sakine Shalikar ,&nbsp;Mohammad Amin Mashayekhpour ,&nbsp;Soheila Ebrahimi Vosta-Kalaee ,&nbsp;Mohaddeseh Abouhosseini Tabari ,&nbsp;Akbar Hajizadeh Moghaddam","doi":"10.1016/j.ibneur.2026.02.008","DOIUrl":"10.1016/j.ibneur.2026.02.008","url":null,"abstract":"<div><div>The purpose of the present investigation is to examine the neuroprotective impact of frankincense at different concentrations (10, 20, and 50 mg/kg/day) and discover its potential mechanisms associated with oxidative stress and apoptosis. To cause Parkinson’s disease (PD) in mice, Paraquat (PQ) was dissolved in 0.9 % normal saline (10 mg/kg, i.p.) and administrated twice a week for three weeks. The mice were randomly divided into five cohorts ( n = 10): i) control (CON), ii) PQ (vehicle), iii) PQ + Frankincense (10 mg/kg), (iv) PQ + Frankincense (20 mg/kg), (v) PQ + Frankincense (50 mg/kg). We evaluated the effects of PQ and frankincense on behaviors using the open field test (OFT), rotarod performance test, forced swim test, and bar test. Oxidative stress factors, inflammatory markers, dopamine levels, acetylcholinesterase (AChE) activity, and apoptotic markers were assessed using ELISA and qPCR, respectively. PQ treatment caused abnormalities in motor coordination in the rotarod test, spontaneous motor activity in OFT, duration of immobility time in the forced swim test, and increased oxidative stress and apoptosis by elevating MDA level, mRNA levels of caspase3, and reducing mRNA levels of Bcl-2 and NGF. PQ treatment also reduced dopamine levels and increased AChE activity. Treatment with frankincense at different concentrations (10, 20, and 50 mg/kg/day) improved motor symptoms by inhibiting oxidative stress, inflammation, and apoptosis and elevation of dopamine levels and NGF gene expression in a dose dependent manner. In sum, frankincense exerted an inhibitory impact on the progression of PQ-induced PD model in mice by mitigating oxidative stress, neuroinflammation, and apoptotic cell death.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 276-285"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146170472","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":"Early diabetes impairs visual function in mice through altering neuronal activity in the primary visual cortex","authors":"Yige Zeng ,&nbsp;Chenling Liu ,&nbsp;Hanlu Chen ,&nbsp;Guangwei Xu ,&nbsp;Lixia Feng","doi":"10.1016/j.ibneur.2025.09.006","DOIUrl":"10.1016/j.ibneur.2025.09.006","url":null,"abstract":"<div><div>Diabetes damages both the retina, leading to retinopathy, and the central visual system, resulting in impaired directional selectivity and color vision in patients without retinopathy. Contrast sensitivity (CS) is a fundamental visual function that allows us to distinguish between objects and backgrounds. In this study, diabetic mice were used to observe the effects of early diabetes on the contrast sensitivity function of primary visual cortex (V1) neurons. Funduscopic examination revealed no retinopathy in mice at four weeks of diabetes. Multichannel electrophysiological recordings and interneuronal correlation analysis revealed that V1 neurons in diabetic mice exhibited significantly reduced CS compared to controls. Furthermore, these neuronal responses showed markedly decreased signal-to-noise ratios along with increased response variability. Notably, noise correlation in V1 of diabetic mice was significantly elevated, providing a basis for neuronal perceptual abnormalities in population neuronal coding. Partially, the dysfunction of neuronal populations and individual units in V1 of diabetic mice can be attributed to the disruption of the excitatory/inhibitory balance. In summary, our findings indicate that significant alterations in neuronal contrast sensitivity function occur in the primary visual cortex of diabetic mice prior to observable fundus lesions, reflecting diminished coding capacity in V1 neurons.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 5-13"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145753857","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":"Endurance training mitigates obesity-induced hippocampal impairment by enhancing neurotrophin signalling, synaptic plasticity, and cellular responses in a female rat model","authors":"Tomáš Kuruc ,&nbsp;Karolína Kuchárová ,&nbsp;Alexandra Kisucká ,&nbsp;Mária Ileninová ,&nbsp;Lenka Ihnátová ,&nbsp;Katarína Kiss Bimbová ,&nbsp;Martina Magurová ,&nbsp;Ján Gálik ,&nbsp;Nadežda Lukáčová","doi":"10.1016/j.ibneur.2026.01.006","DOIUrl":"10.1016/j.ibneur.2026.01.006","url":null,"abstract":"<div><div>Obesity-related health issues, including cognitive decline linked to hippocampal neurogenesis and neuroplasticity, are gaining more attention as obesity rates rise worldwide. Physical activity is recognized as a potent stimulator of neurotrophic factors. This study examined the impact of six weeks of treadmill training on hippocampal molecular pathways in adult female Zucker diabetic fatty (obese) and Zucker lean rats. Animals were assigned to either treadmill exercise (n = 10) or sedentary control (n = 10) groups. Endurance training (ET) markedly upregulated mRNA expression of brain-derived neurotrophic factor and its receptor. The PI3K/Akt pathway was upregulated only in the trained lean rats and downregulated in the trained obese group compared with sedentary controls. ET elicited divergent effects on neurotrophin-associated PLCγ/PKC/CAMKII signalling between lean and obese groups. Sedentary obese rats primarily utilized the PLCγ/PKC axis, while both trained groups (lean and obese) showed increased CAMKII expression, associated with enhanced synaptic plasticity and memory. Enhanced synaptophysin mRNA indicated improved synaptogenesis and plasticity following ET. Trained obese rats also exhibited reduced expression of the microglial pro-inflammatory marker Iba1, alongside increased markers of oligodendrocyte regeneration and neurofilament expression. Behavioral assessment via the passive avoidance test demonstrated improved learning and memory in trained obese animals. Collectively, these findings suggest that ET may mitigate obesity-induced hippocampal damage, exert neuroprotection, and enhance hippocampal function.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 125-138"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972911","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":"Case report of stiff - person syndrome and literature review","authors":"Qiongfang Zhang ,&nbsp;MengJie Xia ,&nbsp;Dan Gui ,&nbsp;Jia Wei ,&nbsp;Yongfeng Liu ,&nbsp;Yanhua Gou","doi":"10.1016/j.ibneur.2025.12.006","DOIUrl":"10.1016/j.ibneur.2025.12.006","url":null,"abstract":"<div><h3>Objective</h3><div>Currently, there is no objective evaluation method to measure muscle tension and therapeutic effects in patients with stiff person syndrome (SPS). We aimed to investigate objective evaluation criteria for diagnosis and treatment. We used needle electromyography (EMG) to record muscle electrical signals before and after the diazepam drug trial to diagnose a patient with SPS.</div></div><div><h3>Method</h3><div>We present a patient who was misdiagnosed as having an \"anxiety state\" for more than a decade because of recurrent tension, worry, and intermittent fear, resulting in generalized muscle stiffness and even falls. Conventional needle EMG was performed on the limbs and axial muscles. The changes in muscle electrical signals before and after diazepam drug trials were recorded.</div></div><div><h3>Results</h3><div>EMG revealed a significant increase in spontaneous motor unit potentials in the patient's limbs and axial muscles at rest. After intravenous injection of diazepam, the spontaneous motor unit gradually reduced and ultimately disappeared. Based on these results, anti-antibody testing for SPS was performed one week later. The results revealed a high titer of anti-glutamic acid decarboxylase 65 antibodies (GAD65-Abs) in serum, while anti-amphiphysin antibodies were negative. The diagnosis was confirmed as SPS.</div></div><div><h3>Conclusion</h3><div>Needle EMG is a convenient tool that can provide diagnostic direction for SPS before genetic testing, enabling clinicians to select specific genes for testing and thereby shortening the time required for clinical examination and diagnosis for patients. Additionally, it can be used to verify the efficacy of experimental medications during testing.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 112-118"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972910","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":"Behavioral effects of a chronic envy-like stress paradigm in mice using an adjacent cage model","authors":"Hiroshi Ueno ,&nbsp;Yoshihiro Tanaka ,&nbsp;Eriko Kitano ,&nbsp;Yu Takahashi ,&nbsp;Sachiko Mori ,&nbsp;Shinji Murakami ,&nbsp;Kenta Wani ,&nbsp;Yosuke Matsumoto ,&nbsp;Motoi Okamoto ,&nbsp;Takeshi Ishihara","doi":"10.1016/j.ibneur.2026.01.008","DOIUrl":"10.1016/j.ibneur.2026.01.008","url":null,"abstract":"<div><h3>Background</h3><div>Social comparison and envy are significant psychosocial stressors in humans and are known to be involved in the onset and persistence of psychiatric disorders. However, animal models capable of experimentally reproducing the effects of indirect social comparison without physical contact are limited. In this study, we used a newly developed \"adjacent-cage paradigm\" to investigate whether chronic vicarious exposure to conspecifics in different environments induces envy-like stress in mice.</div></div><div><h3>Methods</h3><div>Male C57BL/6 N mice served as observers, while demonstrator mice were assigned to one of four conditions: (1) an environment enriched with objects, (2) an igloo, (3) a tube, or (4) social isolation. Observers were continuously exposed to these adjacent cages for 21 days. Subsequently, a comprehensive battery of behavioral tests was conducted to assess general health, anxiety-like behavior, spatial memory, social behavior, and depression-like behavior.</div></div><div><h3>Results</h3><div>In the objects condition, a decrease in time spent in the light compartment of the light/dark box indicated an increase in anxiety-like behavior. In the isolation condition, the mean duration per social interaction was shortened, suggesting a qualitative change in social behavior. The igloo condition resulted in reduced immobility time in the forced swim test, suggesting a possible alteration in stress coping behavior. Furthermore, increased nociceptive sensitivity was observed in the hot plate test under both the objects and isolation conditions.</div></div><div><h3>Conclusion</h3><div>Although the envy-like stress paradigm did not affect many behavioral indices, it did cause condition-dependent and limited behavioral changes. This suggests that the paradigm may serve as a novel model for capturing psychological and context-dependent social stress, which differs from conventional physical stress models. Elucidating the neural basis of this paradigm is expected to contribute to the understanding of how social comparison affects mental health in modern society.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 148-159"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022938","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":"TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas","authors":"Zhenyan Shi ,&nbsp;Danke Shen ,&nbsp;Jie Wu,&nbsp;Hai Luo,&nbsp;Shenhao Xie,&nbsp;Duanzheng Cao,&nbsp;Yong Cao,&nbsp;Bin Tang","doi":"10.1016/j.ibneur.2026.01.007","DOIUrl":"10.1016/j.ibneur.2026.01.007","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the mechanisms by which TNKS1 regulates glycolysis and proliferation in glioma.</div></div><div><h3>Methods</h3><div>Cell viability was assessed using the CCK-8 assay. Levels of glucose and lactate were measured using biochemical detection kits. Western blotting was used to detect the expression levels of glycolysis-related proteins, and qPCR was employed to measure the mRNA expression of GLUT1 and HK2. A subcutaneous xenograft tumor model in nude mice was established. After intratumoral injection of drugs, the effects of TNKS1 knockdown on tumor tissues were observed using HE staining and immunohistochemical staining. Western blotting was also used to detect the expression of PTEN and other proteins in glioma tissues.</div></div><div><h3>Results</h3><div>Compared with the control group, TNKS1 knockdown resulted in increased expression of PTEN, decreased expression of PI3K and p-AKT/AKT proteins, reduced cell proliferation capacity, and lower glucose uptake and lactate production. The results were opposite in the TNKS1 overexpression group. In the group treated with a PI3K agonist compared with the untreated group, the expression of PI3K and p-AKT/AKT proteins increased, and cell proliferation capacity, glucose uptake, and lactate production also increased to varying degrees. In the TNKS1 overexpression + PI3K inhibitor group compared with the TNKS1 overexpression group, the expression of PI3K and p-AKT/AKT proteins decreased, and cell proliferation capacity, glucose uptake, and lactate production also decreased to varying degrees. In the in vivo experiments, compared with the control group, the TNKS1 knockdown group showed increased tumor cell apoptosis and necrosis. Immunohistochemical and Western blotting analyses indicated that compared with the TNKS1-siRNA empty vector group, the TNKS1-siRNA group had significantly increased PTEN protein expression. The expression levels of PI3K, p-AKT/AKT proteins, and Ki67 were significantly lower in the TNKS1-siRNA group, inhibitor group, and TNKS1-siRNA + inhibitor group.</div></div><div><h3>Conclusion</h3><div>TNKS1 regulates glycolysis and proliferation in glioma by mediating the PTEN-PI3K/AKT pathway.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 186-195"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146074242","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":"Norepinephrine and dopamine Imbalance in the medial frontal gyrus from patients with Alzheimer's disease","authors":"Zuleyha Nihan Yurtsever ,&nbsp;Silvia Capuani ,&nbsp;Michela Fratini ,&nbsp;Charles Nicaise ,&nbsp;Yasmine Salman ,&nbsp;Bernard Hanseeuw ,&nbsp;Giovanni Augusto Carlesimo ,&nbsp;Emanuele Claudio Latagliata ,&nbsp;Roberto Coccurello","doi":"10.1016/j.ibneur.2026.01.001","DOIUrl":"10.1016/j.ibneur.2026.01.001","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate catecholaminergic alterations in the medial frontal gyrus (MFG) in Alzheimer’s disease (AD) patients, including a case with TDP-43 pathology, with a focus on norepinephrine (NE) and dopamine (DA) signaling.</div></div><div><h3>Methods</h3><div>Postmortem MFG tissue from five human donors, one with AD, one with AD and TDP-43 co-pathology (AD-TDP43), one preclinical AD, and two controls, was analyzed using high-performance liquid chromatography. Concentrations of NE, DA, and their primary metabolites (MHPG, DOPAC, HVA) were measured to assess neurotransmitter levels and turnover ratios.</div></div><div><h3>Results</h3><div>Elevated MHPG levels were observed only in AD and AD-TDP43 patients, despite unchanged NE concentrations, indicating increased NE turnover. DA levels were also selectively elevated in AD and AD-TDP43 brains only. Possible impaired DA metabolism appeared consistent with reduced DOPAC/DA and HVA/DA ratios and DA turnover.</div></div><div><h3>Conclusions</h3><div>Catecholaminergic dysfunction, marked by increased NE turnover and elevated DA levels, characterizes both AD and AD-TDP43 pathology in the MFG, implicating catecholamine imbalance in disease mechanisms.</div></div><div><h3>Significance</h3><div>By revealing a selective increase in NE turnover and DA levels in the medial frontal lobe, these data may help to clarify the neurochemical imbalance linking cortical to subcortical neurodegeneration, such as that of the locus coeruleus and ventral tegmental area, to catecholamine innervation of the frontal cortex.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 94-100"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145922388","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":"Burden of stroke in China: A decomposition analysis investigating the driven factors","authors":"Lijuan Fu ,&nbsp;Wencai Jiang ,&nbsp;Yanhua Peng ,&nbsp;Xianjie Zhang ,&nbsp;Rui Zhou","doi":"10.1016/j.ibneur.2026.01.012","DOIUrl":"10.1016/j.ibneur.2026.01.012","url":null,"abstract":"<div><h3>Background</h3><div>While the degree of population aging is increasing, a nationwide stroke program was started in 2011. We analyzed how population aging outpaced gains in stroke care in China.</div></div><div><h3>Methods</h3><div>The number of deaths, incidence, prevalence, Disability-Adjusted Life Years (DALYs) attributable to stroke and its subtypes from 2012 to 2021 were extracted from the Global Health Data Exchange database. The total populations of age groups in 2012 and 2021 were extracted from the National Bureau of Statistics of China. The Das Gupta Decomposition method was applied to identify the contributions of population growth, population aging, and the changes in the incidence, mortality, prevalence, and DALYs.</div></div><div><h3>Result</h3><div>From 2012–2021, the total stroke incidence increased by 38.4 % (from 2.95 to 4.09 million), deaths by 17.6 % (from 2.20 to 2.59 million), and prevalence by 34.2 % (from 19.62 to 26.34 million) in China. Decomposition analysis identified rapid population aging as the predominant driver, accounting for 78.1 % of the incidence increase and even exceeding the total death increase (197.6 %), overwhelming the benefits from improved stroke care. The stroke subtype profile shifted markedly, with ischemic stroke's share of incidence rising from 62 % to 68 % and deaths from 41 % to 46 %, while intracerebral hemorrhage's contribution declined.</div></div><div><h3>Conclusion</h3><div>The escalating stroke burden in China is primarily driven by population aging, followed by population growth, creating a paradox where healthcare improvements are offset demographically. The epidemic is increasingly characterized by ischemic stroke, leading to a growing population of survivors requiring long-term care. This necessitates a paradigm shift in health policy from a focus solely on reducing acute mortality towards building cost-effective, integrated systems for lifelong stroke management, chronic care, and secondary prevention tailored for an aging society.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 181-185"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146074129","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":"Structural remodeling of medium spiny neurons in the tail of the striatum and stress-related behavioral alterations after early handling and adolescent stress in male rats","authors":"Negar Kayedi-Bakhtiari,&nbsp;Jafar Vatanparast","doi":"10.1016/j.ibneur.2026.01.004","DOIUrl":"10.1016/j.ibneur.2026.01.004","url":null,"abstract":"<div><div>The tail of the striatum (TS), the most distal part of the striatum, integrates sensory and value-based information and plays a critical role in threat responses. However, its vulnerability to stress remains underexplored. Here, we examined the effects of early handling (EH), chronic social defeat stress (SD) in late adolescence, and their combination (EH-SD) on anxiety- and depression-like behaviors, as well as dendritic morphology and spine density of TS medium spiny neurons (MSNs) in male rats. SD induced anxiety- and depression-like behaviors in the elevated plus maze and forced swim test, whereas EH conferred resilience against these effects. Structural analysis of Golgi-Cox–stained MSNs revealed that EH and EH-SD increased average dendritic process length without affecting branching or total dendritic length. SD markedly elevated dendritic spine density, while EH reduced it; combined EH-SD prevented the SD-induced increase. Although the changes in the total length of dendritic spines in MSNs did not reach a significant level between groups, there was a trend towards increase in the EH and EH-SD groups and a decrease in the SD group, leading to an estimate of the total number of MSN spines did not differ between groups. It seems that EH promotes structural adaptations linked to circuit stabilization, whereas SD enhances excitatory connectivity of TS MSNs, potentially heightening sensitivity to stress-related sensory inputs. Together, the findings identify the TS as a critical site of structural plasticity in stress and early-life experience, and suggest a link between MSN morphology and resilience or vulnerability to stress-related behavioral outcomes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"20 ","pages":"Pages 101-111"},"PeriodicalIF":2.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972913","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}