Journal of integrative neuroscience最新文献

{"title":"Before HSP40 Polymorphisms Are Held Responsible for an Increased Stroke Risk, All Other Influencing Factors Must Be Excluded.","authors":"Sounira Mehri, Josef Finsterer","doi":"10.31083/JIN37265","DOIUrl":"https://doi.org/10.31083/JIN37265","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"37265"},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015530","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":"Sleep Paralysis: Pathogenesis, Clinical Manifestations, and Treatment Strategies.","authors":"Yi'an Wang, Qi Li, Zhijun Zhong, Qian Ouyang, Xueliang Zou, Kaiyu Yue, Dongyuan Yao","doi":"10.31083/JIN38979","DOIUrl":"https://doi.org/10.31083/JIN38979","url":null,"abstract":"<p><p>Sleep paralysis, colloquially known as \"ghost pressing\" is a state of momentary bodily immobilization occurring either at the onset of sleep or upon awakening. It is characterized by atonia during rapid eye movement (REM) sleep that continues into wakefulness, causing patients to become temporarily unable to talk or move but possessing full consciousness and awareness of their surroundings. Sleep paralysis is listed in the International Classification of Sleep Disorders, 3rd Edition (ICSD-3) as a parasomnia occurring during REM sleep that be classified as either isolated or narcolepsy-associated. Several brain areas, including the forebrain, hypothalamus, and brainstem, as well as several neurotransmitters and modulators, are involved in the control of REM sleep. The primary brain region responsible for inducing muscle paralysis during REM sleep is the subcoeruleus nucleus, also known as the sublaterodorsal (SLD) nucleus in rats. Sleep paralysis results from the inability to immediately restore muscle tone during the transition from sleep to wakefulness. In this article, we systematically review the neural circuit that controls REM sleep and the underlying mechanisms, predisposing factors, clinical characteristics, and treatments for sleep paralysis. We also compare isolated sleep paralysis (ISP) and narcolepsy-associated sleep paralysis and speculate upon the role of microsleep in sleep paralysis.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"38979"},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015588","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":"Reply to Comment on Josef H. Finsterer, <i>et al</i>. \"Polymorphism in Genes Encoding HSP40 Family Proteins is Associated With Ischemic Stroke Risk and Brain Infarct Size: A Pilot Study. Journal of Integrative Neuroscience. 2024;23(12):211\".","authors":"Ksenia A Kobzeva, Denis E Gurtovoy, Alexey V Polonikov, Vladimir M Pokrovsky, Evgeny A Patrakhanov, Olga Y Bushueva","doi":"10.31083/JIN43297","DOIUrl":"https://doi.org/10.31083/JIN43297","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"43297"},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015582","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":"Brain Insulin Signaling Pathway Regulation of Hippocampal Neuroplasticity in Neurocognitive Disorders: Mechanisms and Therapeutic Implications.","authors":"Yanan He, Miao Sun, Mengyao Qu, Yixun Lu, Huikai Yang, Rui Wang, Yingfu Li, Peng Li, Weidong Mi, Yulong Ma","doi":"10.31083/JIN39446","DOIUrl":"https://doi.org/10.31083/JIN39446","url":null,"abstract":"<p><p>Neurocognitive disorders represent a significant global health challenge and are characterized by progressive cognitive decline across conditions including Alzheimer's disease, mild cognitive impairment, and diabetes-related cognitive impairment. The hippocampus is essential for learning and memory and requires intact neuroplasticity to maintain cognitive function. Recent evidence has identified the brain insulin signaling pathway as a key regulator of hippocampal neuroplasticity through multiple cellular processes including synaptic plasticity, neurotransmitter regulation, and neuronal survival. Dysregulation of this pathway contributes substantially to the pathophysiology of cognitive dysfunction in various disorders. Mechanistically, insulin modulates hippocampal neuroplasticity primarily through the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) cascades, both of which promote synaptic plasticity and support neurogenesis. Beyond its neuronal effects, insulin signaling also regulates glial and endothelial cell function, orchestrating a coordinated multicellular response that is critical for hippocampal integrity. Emerging therapeutic approaches that target this pathway include intranasal insulin administration, glucagon-like peptide-1 (GLP-1) receptor agonists, and peroxisome proliferator-activated receptor (PPAR) agonists. These have demonstrated promising efficacy in restoring hippocampal function and improving cognitive outcomes in both preclinical and clinical studies. This review synthesizes current knowledge on the relationship between brain insulin signaling and hippocampal neuroplasticity. In addition, we highlight the therapeutic potential of insulin-targeted interventions for neurocognitive disorders, including quantifiable outcomes and sex-specific considerations.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39446"},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015552","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":"Nasal Cytology and Clinical Rhinology Support a Translational Integrative Neuroscience Perspective.","authors":"Wael Abu Ruqa, Martina Romeo, Gianluca Cipolloni, Davide Rosati, Camilla Laureti, Stefano Venarubea, Fabrizio Liberati, Alessandro Santirocchi, Carla Petrella, Carlo Cogoni, Vincenzo Cestari, Christian Barbato, Antonio Minni","doi":"10.31083/JIN33392","DOIUrl":"https://doi.org/10.31083/JIN33392","url":null,"abstract":"<p><p>Nasal cytology is evolving into a promising tool for diagnosing neurological and psychiatric disorders, especially those such as Alzheimer's and Parkinson's diseases. Moreover, recent research has indicated that biomarkers differ greatly between samples taken before and after death. Nasal cytology might help to identify the early stages of cognitive decline. The association of olfactory disturbances with a host of these neurological disorders is remarkable. This means that the nose, something we probably take for granted, could well be the best means of establishing important biomarkers for earlier diagnoses in these conditions. The nose is a source of epithelial and neuroepithelial cells that can be used in <i>in vitro</i> cultured models and nasal cytology provides new avenues for translational, integrative neuroscientific research. The future incorporation of artificial intelligence into cytological analyses would facilitate the acceptance of nasal cytology as a screening platform for neurodegenerative and psychiatric conditions, facilitating early diagnosis and better management for patients.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"33392"},"PeriodicalIF":2.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015585","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":"Inhibition of cGAS Reduces Brain Injury and Facilitates Neurological Recovery via the STING-Mediated Signaling Pathway After Germinal Matrix Hemorrhage in Neonatal Mice.","authors":"Yiheng Wang, Xuhui Yin, Xiaoli Zhang, Xixiao Zhu, Yiting Luo, Bing-Qiao Zhao","doi":"10.31083/JIN39286","DOIUrl":"10.31083/JIN39286","url":null,"abstract":"<p><strong>Background: </strong>Germinal matrix hemorrhage (GMH) is a common complication of premature infants with lifelong neurological consequences. Inflammation-mediated blood-brain barrier (BBB) disruption has been implicated as a main mechanism of secondary brain injury after GMH. The cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a crucial role in inflammation, yet its involvement in GMH pathophysiology remains unclear.</p><p><strong>Methods: </strong>Collagenase was injected into the right germinal matrix of postnatal day 5 (P5) mouse pups to induce GMH. Either RU.521, or RU.521 combined with a STING agonist SR-717 was administered to the mice after GMH. The number of microglia, proinflammatory cytokines, microglial polarization, BBB permeability, demyelination, and axon degeneration were analyzed by immunofluorescence staining, western blotting, and quantitative real-time PCR. Neurobehavioral functions were evaluated using novel object recognition, Y-maze, and rotarod tests.</p><p><strong>Results: </strong>After induction of GMH, cGAS and STING were upregulated in the peri-hematomal area with a peak at 24 h, and they were mainly expressed in microglia. RU.521 treatment decreased the number of microglia, proinflammatory cytokines and microglial polarization, preserved BBB integrity, and decreased its permeability after GMH. Moreover, RU.521 decreased GMH-mediated upregulation of STING, phosphorylated TANK-binding kinase 1 (phospho-TBK1), phosphorylated interferon regulatory factor 3 (phospho-IRF3), and interferon-β (IFN-β), diminished demyelination, axon degeneration, and neurological deficits. The STING agonist SR-717 blunted RU.521-induced downregulation of phospho-TBK1, phospho-IRF3 and IFN-β and blocked RU.521-mediated inhibition of inflammation, protected against BBB breakdown, white matter lesions, and neurological dysfunction after GMH.</p><p><strong>Conclusions: </strong>Inhibition of cGAS improved white matter lesions and neurological dysfunction by modulating the microglial polarization towards decreased neuroinflammation and maintaining BBB integrity through STING-mediated type I IFN-β production. Thus, cGAS may be a potential therapeutic target for the treatment of GMH.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39286"},"PeriodicalIF":2.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015604","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":"Glucocorticoid Alleviates Stress-induced Hypothalamic Nerve Injury by Inhibiting the GSDMD-dependent Pyroptosis Pathway.","authors":"Shanyong Yi, Lijie Zhu, Yaxin Guo, Bin Zhao, Lai Wei, Zhijun Yao, Bin Yang","doi":"10.31083/JIN39532","DOIUrl":"https://doi.org/10.31083/JIN39532","url":null,"abstract":"<p><strong>Background: </strong>Excessive stress leads to stress injury but the underlying mechanism is not completely understood and current preventive protocols are inadequate. This study aimed to investigate if glucocorticoid (GC) reduces nerve damage in the hypothalamus caused by stress and to clarify the mechanisms involved.</p><p><strong>Methods: </strong>Behavioral alterations in stressed rats were observed using the open field test. Changes in the levels of stress hormones, inflammatory factors, and stress-related injury factors were detected using enzyme-linked immunosorbent assay (ELISA). Pathological alterations in the hypothalamus were observed using thionine staining and hematoxylin & eosin (HE) staining. The expression levels of proteins linked to pyroptosis were determined using western blotting.</p><p><strong>Results: </strong>Stressed rats presented obvious anxiety-like behavior; the levels of stress hormones, inflammatory factors, and injury-related factors fluctuated abnormally. Morphological findings indicated substantial damage in the hypothalamus. Stress-induced nerve injury was alleviated by low-dose GC treatment, which also dramatically decreased the concentrations of inflammation-associated markers and expression of the gasdermin D (GSDMD)-related pyroptosis pathway.</p><p><strong>Conclusions: </strong>Low-dose GC alleviates hypothalamic nerve injury by inhibiting the GSDMD-dependent pyroptosis pathway in stressed rats.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 8","pages":"39532"},"PeriodicalIF":2.7,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015567","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":"Inactivation of Dorsolateral Prefrontal Cortex During Auditory Working Memory.","authors":"Bethany Plakke, Katryna Skye Kevelson, Charles Leyens, Lizabeth M Romanski","doi":"10.31083/JIN38877","DOIUrl":"https://doi.org/10.31083/JIN38877","url":null,"abstract":"<p><strong>Background: </strong>The dorsolateral prefrontal cortex (DLPFC) is a critical node in the working memory (WM) neural circuit, established through neurophysiology, neuropsychology, and neuroimaging studies in humans and nonhuman primates. While most of the neurophysiological evidence for the role of the DLPFC in WM comes from visuospatial WM paradigms, evidence for its role in auditory WM has been suggested by the fact that large lateral prefrontal cortex lesions in nonhuman primates cause auditory discrimination deficits. Moreover, DLPFC neurons demonstrate task-related neuronal responses during auditory WM. In contrast, other studies have proposed that the ventrolateral prefrontal cortex (VLPFC) plays a pivotal role in auditory and audiovisual processing, integration, and mnemonic processing, since VLPFC neurons are responsive to complex acoustic stimuli and are robustly active during auditory WM tasks. Furthermore, inactivation of the VLPFC impairs audiovisual and auditory WM. In these inactivation studies the cortical region that was inactivated by cortical cooling included areas 12/47, 45 and 46 ventral. It is possible that inclusion of area 46 ventral may account for the auditory WM performance deficit previously observed while inactivating VLPFC so further experiments are needed.</p><p><strong>Methods: </strong>In the present study we examined whether transient inactivation of the DLPFC, including areas 46v and 46d, and 9, in rhesus macaques would effect auditory WM. The DLPFC was inactivated by cortical cooling while two rhesus macaques performed an auditory working memory task. This was followed by permanent ibotenic acid lesions and assessment of behavioral performance post-lesion.</p><p><strong>Results: </strong>Our experiments demonstrated that inactivation of DLPFC by cortical cooling in two macaques did not result in a significant decrease in performance of an auditory WM task. The inactivation resulted in an increase in dropped gaze events during the latter half of the task, in one subject, which could be due to a loss of attention or motivation. The ibotenic acid lesions of the DLPFC did not significantly alter performance on the auditory WM task.</p><p><strong>Conclusions: </strong>Our results showed that DLPFC transient inactivation with cortical cooling and ibotenic acid lesions did not significantly alter overall auditory working memory performance, which differs from the impairment seen when the VLPFC is inactivated. Our data suggest that the DLPFC and VLPFC may play different roles in auditory working memory.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 7","pages":"38877"},"PeriodicalIF":2.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789330","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":"Response to Questions Regarding \"Altered Resting-State Electroencephalogram Microstate Characteristics in Stroke Patients\".","authors":"Hao-Yu Lu, Zhen-Zhen Ma, Jun-Peng Zhang, Jia-Jia Wu, Mou-Xiong Zheng, Xu-Yun Hua, Jian-Guang Xu","doi":"10.31083/JIN42715","DOIUrl":"https://doi.org/10.31083/JIN42715","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 7","pages":"42715"},"PeriodicalIF":2.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789246","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":"All Factors Influencing Microstate Changes in Stroke Patients must be Taken into Account before the Stroke is Blamed as the Only Determinant.","authors":"Josef Finsterer, João Gama Marques","doi":"10.31083/JIN28266","DOIUrl":"https://doi.org/10.31083/JIN28266","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 7","pages":"28266"},"PeriodicalIF":2.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144789322","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}