Brain Research Bulletin最新文献

{"title":"Expression of concern: \"Electrical stimulation of olfactory bulb downregulates RGMa expression after ischemia/reperfusion injury in rats\" [BRAIN RES BULL, Volume 86 (2011) 254-261].","authors":"","doi":"10.1016/j.brainresbull.2025.111379","DOIUrl":"10.1016/j.brainresbull.2025.111379","url":null,"abstract":"","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"111379"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293309","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":"Glial cell crosstalk in the local microenvironment following spinal cord injury","authors":"Erliang Li ,&nbsp;Yingchao Gao ,&nbsp;Jianfeng Zhang ,&nbsp;Peng Zou ,&nbsp;Huanhuan Qiao ,&nbsp;Rui Zhang ,&nbsp;Yansheng Huang","doi":"10.1016/j.brainresbull.2025.111436","DOIUrl":"10.1016/j.brainresbull.2025.111436","url":null,"abstract":"<div><div>Spinal cord injury (SCI) has a high incidence, significant rates of disability, and substantial economic costs. The response of glial cells is crucial for spinal cord regeneration following SCI. However, the roles of various glial cell types in SCI pathology and their interactions with other cellular targets remain poorly understood. Using single-cell RNA sequencing, we characterized the local microenvironment following SCI and isolated three glial cell types—microglia, astrocytes, and oligodendrocytes—at the injury site. Immunofluorescence confirmed the differential expression of these cell types in spinal cord tissues. Four subtypes of microglia were identified: activated, dividing, homeostatic, and inflammatory. Astrocytes were categorized into 11 clusters, while oligodendrocytes were classified into eight clusters. Enrichment analysis indicated that the loss of oligodendrocytes was associated with ferroptosis. The glial cell crosstalk network revealed various interactions, including TIMP1-FGFR2 and PLXNB2-PTN in astrocytes and oligodendrocytes, as well as LGALS3-MERTK, GPR37L1-PSAP, TFRSF1A-GRN, and PGRMC2-CCL4L2 in astrocytes and microglia. A total of 75 drugs were identified through target-drug screening. This study suggests potential differentiation and intricate crosstalk among these three cell types, provides a theoretical framework for simulating the glial cellular microenvironment of SCI, and establishes a foundation for future interventions aimed at targeting various glial cell processes in the treatment of SCI.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111436"},"PeriodicalIF":3.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322887","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":"Postoperative Loss of Perineuronal Nets in the Hippocampal CA1 Region Results in Memory Consolidation Deficits.","authors":"Zun-Sai Feng, Jiang-Nan Wu, Gui-Cheng Wang, Zi-Qing Xu, Yan-Jing Guo, Shi-Yu Hao, Gong-Ming Wang, Meng-Yuan Zhang","doi":"10.1016/j.brainresbull.2025.111433","DOIUrl":"https://doi.org/10.1016/j.brainresbull.2025.111433","url":null,"abstract":"<p><p>Postoperative cognitive dysfunction (POCD) is a common postoperative neurological complication, with memory consolidation deficits being one of its prominent features. However, the mechanisms underlying postoperative memory consolidation deficits are still unclear. The perineuronal net (PNN) is a specialized extracellular matrix that predominantly surrounds parvalbumin (PV) interneurons and is closely associated with cognitive functions, including learning and memory. Theta oscillations in the hippocampal CA1 region are crucial for memory consolidation. However, the relationships among postoperative memory consolidation deficits, theta oscillation abnormalities, and PNNs remain unclear. The aim of this study was to investigate the role of PNNs in the CA1 region in postoperative memory consolidation deficits and theta oscillation abnormalities. The experiments revealed that, after anesthesia and surgery, the mice exhibited memory consolidation deficits, abnormal theta oscillations, and PNNs loss in the hippocampal CA1 region. Increasing the density of PNNs alleviated postoperative memory consolidation deficits and theta oscillation abnormalities. In contrast, normal mice treated with chondroitinase ABC (ChABC) to degrade PNNs presented a similar phenotype of postoperative memory consolidation deficits. Further investigations revealed that PNNs loss in surgical mice weakened the inhibitory function of PV interneurons. Increase the density of PNNs reversed these changes, while ChABC degradation of PNNs also weakened the inhibitory function of PV interneurons. Notably， PNNs loss after surgery was associated with increased microglial phagocytosis. In conclusion, the PNNs loss caused by increased microglial phagocytosis in the hippocampal CA1 region after surgery palys an important role in postoperative memory consolidation deficits and theta oscillation abnormalities, which is associated with the impaired function of PV interneurons. This study provides new theoretical insights and potential targets for preventing and treating postoperative memory consolidation deficits.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"111433"},"PeriodicalIF":3.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339903","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":"Left-right confusion in psychiatric, neurodevelopmental and neurological disorders: A systematic review","authors":"Moritz Thaler ,&nbsp;Sebastian Ocklenburg","doi":"10.1016/j.brainresbull.2025.111435","DOIUrl":"10.1016/j.brainresbull.2025.111435","url":null,"abstract":"<div><div>Left-right confusion is common in healthy individuals, but increased prevalence has been reported in several psychiatric, neurodevelopmental, and neurological disorders. The present systematic review aimed to identify disorders in which the prevalence of left-right confusion is higher than in the general population. For this purpose, a systematic review following PRISMA guidelines was conducted using the databases Google Scholar, PubMed, and Mendeley. A total of 20 quantitative case-control studies were included. Lesions in parietal brain areas and damage to temporal-parietal-occipital brain areas because of Alzheimer's disease were associated with severe impairments in left-right orientation. Furthermore, evidence for developmental impairments in direction assignment was provided by studies on developmental topographical disorientation (DTD). These DTD-related impairments are associated with low functional connectivity between the hippocampus and the right prefrontal cortex. Individuals with DTD show significantly poorer performance in direction discrimination compared to healthy subjects. In addition, the review highlights that, despite previous research, there remains a substantial need for further studies and for the development of a uniform definition and operationalization of left-right confusion in clinical populations.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111435"},"PeriodicalIF":3.5,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330937","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 unique role of the associative thalamus in cognitive processing","authors":"Bin A. Wang ,&nbsp;Shumei Li ,&nbsp;Michael M. Halassa ,&nbsp;Burkhard Pleger","doi":"10.1016/j.brainresbull.2025.111432","DOIUrl":"10.1016/j.brainresbull.2025.111432","url":null,"abstract":"<div><div>The thalamus, centrally located in the forebrain, has traditionally been recognized as a relay station for sensory and motor signals. Recent research has challenged this perspective by revealing previously unrecognized functions, such as regulating cortical excitability, maintaining the balance between excitation and inhibition, and modulating effective connectivity. These non-relay functions stem from genuine thalamic processing of a wide range of inputs that lead to contextual signals that play a role in advanced cognitive abilities underpinning learning, attention, and executive functions. Particularly, associative thalamic structures, such as the mediodorsal thalamus and pulvinar which receive driving inputs from the cortex and participate in transthalamic cortico- cortical loop, play a crucial role in enhancing information processing efficiency for higher cognitive functions. This paper reviews recent advances in thalamic research, with a focus on the pulvinar and mediodorsal thalamus and their integrative role in cognitive processing. We discuss the computational principles of these transthalamic interactions revealed by the neural network models. We additionally summarize recent evidence on how thalamic dysfunctions contribute to mental disorders, using schizophrenia as a key example, and highlight the potential of targeting the associative thalamus for novel diagnostic and therapeutic strategies. This review combines findings from both animal models and human studies, providing a comprehensive overview of the diverse contributions of the thalamus to cognition and its potential to revolutionize mental health treatment through a multidisciplinary perspective.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111432"},"PeriodicalIF":3.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144290715","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":"METTL3-YTHDF1 axis drives BCL-3 m6A methylation to promote the ferroptosis of brain microvascular endothelial cells during intracerebral hemorrhage","authors":"Hao Yin,&nbsp;Zhongying Ran,&nbsp;Tao Luo,&nbsp;Zexin Jin,&nbsp;Ying Tan,&nbsp;Jun Ma","doi":"10.1016/j.brainresbull.2025.111434","DOIUrl":"10.1016/j.brainresbull.2025.111434","url":null,"abstract":"<div><div>Intracerebral hemorrhage (ICH) significantly impacts human health, with emerging evidence indicating that N6-methyladenosine (m⁶A) modifications serve a critical regulatory function in ischemic stroke. However, the underlying mechanisms remain largely unexplored. This study sought to comprehensively analyze aberrant m⁶A modification and its mechanistic implications following ICH. Differential expression of BCL-3 between Sprague-Dawley rat ICH models and control rats was identified through analysis of methylated RNA Immunoprecipitation and RNA sequencing data, revealing a close association with methyltransferase-like 3 (METTL3), an m⁶A methyltransferase. METTL3 knockdown and overexpression were conducted in an <em>in vitro</em> ICH model to further elucidate the roles of METTL3 and BCL-3 in apoptosis and ferroptosis. The results indicated that METTL3 knockdown significantly reduced BCL-3 expression, inhibited reactive oxygen species production, and decreased apoptosis and ferroptosis. Conversely, METTL3 overexpression resulted in the opposite effects. BCL-3 overexpression mitigated the effects induced by METTL3 knockdown. Moreover, YTHDF1 knockdown resulted in outcomes comparable to those observed following METTL3 knockdown. <em>In vivo</em> experiments demonstrated that METTL3 knockdown inhibited ferroptosis and protected brain tissue, whereas BCL-3 overexpression exacerbated brain damage. In conclusion, our findings suggest that BCL-3 expression, regulated by METTL3- and YTHDF1-mediated methylation, promotes apoptosis and ferroptosis following ICH, thereby contributing to neuronal injury. This study reveals a novel epitranscriptomic regulatory pathway involved in ICH pathology and identifies the METTL3-YTHDF1-BCL-3 axis as a promising therapeutic target for mitigating neuronal damage post-ICH.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111434"},"PeriodicalIF":3.5,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307644","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":"Exploring the links between functional activation and hallucination proneness","authors":"Abdullah M. Alotaibi ,&nbsp;Manal H. Alosaimi ,&nbsp;Razan S. Orfali ,&nbsp;Mansour Alshanawani ,&nbsp;Richard Bentall ,&nbsp;Georg Meyer","doi":"10.1016/j.brainresbull.2025.111424","DOIUrl":"10.1016/j.brainresbull.2025.111424","url":null,"abstract":"<div><div>Hallucinations are often associated with alterations in brain activation, particularly in language-related and sensory processing areas. Existing models suggest different frameworks for understanding the relationship between brain activation and hallucination proneness, yet practical evidence supporting these models remains limited. This study investigates the neural correlates of hallucination proneness in healthy individuals through functional MRI (fMRI) tasks focusing on both auditory and visual processing, including voice and text comprehension, face recognition, and audio-visual stimuli. Participants, primarily university students, completed Launay-Slade Hallucination Scale–Modified (LSHS-M) measures, including auditory (LSHS-A) and visual (LSHS-V) subscales, while undergoing fMRI scans. Correlations were examined between hallucination proneness scores and brain activation in task-relevant and task-irrelevant regions. Although no significant correlations were found between hallucination scores and activation in task-relevant areas, positive correlations emerged in language-related regions during visual tasks, suggesting increased engagement in task-irrelevant areas. These results point to an inhibition deficit in individuals with higher hallucination proneness, supporting theories of reduced cognitive control. Furthermore, lateralization indices showed no significant correlation with hallucination scores, challenging assumptions about the continuum hypothesis in non-clinical populations. Taken together, these findings highlight the complexity of the neural mechanisms underlying hallucination proneness. While the study provides partial support for inhibition-based theories, the largely null results highlight the need for sensitive tasks, robust statistical controls, and broader populations to fully elucidate the neurobiological basis of hallucination proneness.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111424"},"PeriodicalIF":3.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298139","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":"Activation of cannabinoid CB1 receptors suppresses HCN channels function in dorsal root ganglion neurons of rats","authors":"Xiaolu Lei ,&nbsp;Meiyun Chen ,&nbsp;Xingfeng Liu ,&nbsp;Yan Yan ,&nbsp;Xupeng Li ,&nbsp;Fei Gong ,&nbsp;Deqian Yu ,&nbsp;Xiaohong Liu","doi":"10.1016/j.brainresbull.2025.111425","DOIUrl":"10.1016/j.brainresbull.2025.111425","url":null,"abstract":"<div><div>Cannabinoid receptor (CBR) and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are both critically involved in pain hypersensitivity induced by nerve injury. Both CBR and HCN channels are expressed in sensory neurons of the dorsal root ganglia (DRG). Studies have shown that HCN channel function is regulated by cAMP-PKA signaling, and the activation of cannabinoid receptor 1 (CB1R) can inhibit cAMP-PKA activity. However, it remains unclear whether the function of HCN channels is regulated by CB1R activity in DRG. In this study, we investigated the effect of ACEA, a selective agonist for CB1R, on HCN channel expression and function in the DRG of rats with chronic constriction injury (CCI) of the sciatic nerve. Mechanical allodynia was assessed by measuring the mechanical withdrawal threshold (MWT). HCN1/ HCN2 channel expression and cAMP level in lumbar 4, 5 and 6 (L4–6) DRG were detected by Western blot analysis and ELISA, respectively. As a result, MWT decreased significantly in CCI rats. HCN1/ HCN2 channel expression and cAMP level increased in the ipsilateral L4–6 DRG after CCI operation. Notably, intrathecal injection of ACEA (0.05 mg/kg) significantly decreased mechanical allodynia, HCN1/ HCN2 expression, and cAMP level in CCI rats, and this effect was blocked by the CB1R antagonist AM251. On the other hand, I_h mediated by HCN channels of DRG neurons was recorded by whole-cell patch-clamp to evaluate HCN channel activity. In this assay, ACEA (1 μM) significantly reduced the amplitude of I_h in DRG neurons (<em>P</em> &lt; 0.01), while pretreatment with AM251 blocked the inhibitory effect of ACEA on I_h (<em>P</em> &lt; 0.01). In addition, 8-Br-cAMP, a PKA activator, could reverse the effect of ACEA on I_h in DRG neurons (<em>P</em> &lt; 0.01), indicating that CB1R activation suppresses the function of HCN channels by decreasing cAMP-PKA activity. In conclusion, these findings suggest that CB1R activation can inhibit the function of HCN channels by decreasing cAMP-PKA activity, resulting in decreased excitability of primary sensory neurons.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111425"},"PeriodicalIF":3.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144272154","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":"Arecoline alleviates autism spectrum disorder-like behaviors and cognition disorders in a valproic acid mouse model by activating the AMPK/CREB/BDNF signaling pathway","authors":"Chunyan Wen ,&nbsp;Zhizhong Xu ,&nbsp;Fengling Cao,&nbsp;Qianfa Yuan,&nbsp;Weichao Su,&nbsp;Zhiyuan Huang","doi":"10.1016/j.brainresbull.2025.111431","DOIUrl":"10.1016/j.brainresbull.2025.111431","url":null,"abstract":"<div><div>Studies in humans have revealed that the pathogenesis of autism spectrum disorder (ASD) is linked to white matter abnormalities involving hypomyelination and oligodendroglia dysfunction; however, effective treatments remain limited. Similarly, the valproic acid (VPA) model mice, which are widely used to study ASD, also exhibit white matter abnormalities with hypomyelination. Arecoline has been reported to enhance memory and cognition, facilitate myelination and improve neurological function. This study investigated the therapeutic potential of arecoline in a mouse model of prenatal VPA-induced ASD. We established an ASD mouse model through prenatal exposure to VPA and treated the mice with arecoline for 4 weeks. Behavioral analyses, including the elevated-plus maze, open field, self-grooming, marble-burying, three-chamber, Y-maze, and Morris water maze tests, were conducted to assess the effects of arecoline on behavior. Western blotting was used to detect changes in protein expression in the frontal cortex after arecoline treatment. The results revealed that offspring prenatally exposed to VPA presented characteristic behavioral abnormalities, including increased repetitive and stereotyped behaviors, deficits in social interaction, and impairments in learning and memory, accompanied by reduced expression of the myelin marker MBP and the mature oligodendrocyte marker GST-pi in the frontal cortex. Four-week arecoline treatment (1 and 2 mg/kg/day) significantly ameliorated these behavioral and cognitive abnormalities and restored myelination markers. Further mechanistic investigations demonstrated that arecoline enhanced the phosphorylation levels of AMPKα and CREB in the frontal cortex. This activation upregulated the expression of downstream BDNF, an essential neurotrophic factor for oligodendrocyte maturation and remyelination. These findings suggest that the AMPK/CREB/BDNF pathway may contribute to the therapeutic effects of arecoline, potentially through increased oligodendrocyte maturation and remyelination. This study provides preclinical evidence supporting arecoline as a potential myelination-targeting intervention, with implications for ASD and other neurological disorders involving myelination deficits.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"229 ","pages":"Article 111431"},"PeriodicalIF":3.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293308","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":"Associations among neuropsychological performance, brain structural alterations, and glymphatic function in patients with minimal hepatic encephalopathy","authors":"Chao Ju ,&nbsp;Longtao Yang ,&nbsp;Zhongshang Dai ,&nbsp;Yisong Wang ,&nbsp;Chang Li ,&nbsp;Wei Zhao ,&nbsp;Yongfang Jiang ,&nbsp;Haiyang Li ,&nbsp;Jun Liu","doi":"10.1016/j.brainresbull.2025.111416","DOIUrl":"10.1016/j.brainresbull.2025.111416","url":null,"abstract":"<div><div>Brain anatomical alterations in gray matter(GM), white matter(WM), and glymphatic system(GS) in patients with hepatitis B cirrhosis(HBC) with minimal hepatic encephalopathy(MHE) remain to be clarified. A total of 33 healthy controls and 37 patients with treatment-native primary HBC (further subdivided into HBC in MHE group[MHE] and HBC in non-MHE group[NMHE]) participated in neuroimaging study with three-dimensional T1 and a half q-space Cartesian grid diffusion model. Group differences in regional GM volume(GMV) were assessed using voxel-based morphometry(VBM) analysis. Differences in WM diffusion metrics were compared using tract-based spatial statistics(TBSS) analysis. Diffusion tensor image analysis along the perivascular space(DTI-ALPS) was employed to evaluate GS function. Compared to healthy control group (HC), GMV was reduced in MHE group, mainly in the vermis, bilateral pallidum, and right putamen, but was increased in right lateral geniculate thalamus(Thal_LGN_R) and left pulvinar medial thalamus(Thal_PuM_L). MHE patients displayed greater isotropic volume fraction(ISOVF) in the right sagittal stratum, right superior longitudinal fasciculus, left fornix(cres)/stria terminalis, left corticospinal tract, left cerebral peduncle, and left cingulum (hippocampus) than HC. DTI-ALPS was significantly downregulated in MHE patients. It revealed cortical changes, low-grade WM edema, and GS disorders at the early stage of chronic HBC, which will aid in MHE identification.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"228 ","pages":"Article 111416"},"PeriodicalIF":3.5,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144222622","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}