Neurobiology of Disease最新文献

{"title":"Corrigendum to “Huntingtin lowering impairs the maturation and synchronized synaptic activity of human cortical neuronal networks derived from induced pluripotent stem cells” [Neurobiology of Disease Volume 200 (2024, Oct 1st) - Article# YNBDI_106630]","authors":"Mathilde Louçã , Donya El Akrouti , Aude Lemesle , Morgane Louessard , Noëlle Dufour , Chloé Baroin , Aurore de la Fouchardière , Laurent Cotter , Hélène Jean-Jacques , Virginie Redeker , Anselme L. Perrier","doi":"10.1016/j.nbd.2024.106703","DOIUrl":"10.1016/j.nbd.2024.106703","url":null,"abstract":"","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106703"},"PeriodicalIF":5.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatially heterogeneous lipid dysregulation in tuberculous meningitis","authors":"John Kim ,&nbsp;Ian Spears ,&nbsp;Clara Erice ,&nbsp;Hye-Young H. Kim ,&nbsp;Ned A. Porter ,&nbsp;Caitlin Tressler ,&nbsp;Elizabeth W. Tucker","doi":"10.1016/j.nbd.2024.106721","DOIUrl":"10.1016/j.nbd.2024.106721","url":null,"abstract":"<div><div>Tuberculous (TB) meningitis is the deadliest form of extrapulmonary TB which disproportionately affects children and immunocompromised individuals. Studies in pulmonary TB have shown that <em>Mycobacterium tuberculosis</em> can alter host lipid metabolism to evade the immune system. Cholesterol lowering drugs (i.e., statins) reduce the risk of infection, making them a promising host-directed therapy in pulmonary TB. However, the effect of <em>M. tuberculosis</em> infection on the young or adult brain lipidome has not been studied. The brain is the second-most lipid-rich organ, after adipose tissue, with a temporally and spatially heterogeneous lipidome that changes from infancy to adulthood. The young, developing brain in children may be uniquely vulnerable to alterations in lipid composition and homeostasis, as perturbations in cholesterol metabolism can cause developmental disorders leading to intellectual disabilities. To begin to understand the alterations to the brain lipidome in pediatric TB meningitis, we utilized our previously published young rabbit model of TB meningitis and applied mass spectrometry (MS) techniques to elucidate spatial differences. We used matrix assisted laser desorption/ionization-MS imaging (MALDI-MSI) and complemented it with region-specific liquid chromatography (LC)-MS/MS developed to identify and quantify sterols and oxysterols difficult to identify by MALDI-MSI. MALDI-MSI revealed several sphingolipids, glycerolipids and glycerophospholipids that were downregulated in brain lesions. LC-MS/MS revealed the downregulation of cholesterol, several sterol intermediates along the cholesterol biosynthesis pathway and enzymatically produced oxysterols as a direct result of <em>M. tuberculosis</em> infection. However, oxysterols produced by oxidative stress were increased in brain lesions. Together, these results demonstrate significant spatially regulated brain lipidome dysregulation in pediatric TB meningitis.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106721"},"PeriodicalIF":5.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased dopamine D2/D3 receptor and serotonin transporter availability in male rats after spontaneous remission from repeated social defeat-induced depression; a PET study in rats","authors":"Rodrigo Moraga-Amaro ,&nbsp;Daniel Aaron Vazquez-Matias ,&nbsp;Luiza Reali Nazario ,&nbsp;Rudi A.J.O. Dierckx ,&nbsp;Jimmy Stehberg ,&nbsp;Janine Doorduin ,&nbsp;Erik F.J. de Vries","doi":"10.1016/j.nbd.2024.106727","DOIUrl":"10.1016/j.nbd.2024.106727","url":null,"abstract":"<div><div>Most pharmacological treatments for depression target monoamine transporters and about 50 % of treated patients attain symptomatic remission. Once remission is attained, it is hard to distinguish the changes on brain monoaminergic transmission induced by the antidepressants, from those associated to remission <em>per se</em>. In this study, we aimed at studying the brain of spontaneously remitted rats from repeated social defeat (RSD)-induced depression in terms of dopamine D₂/D₃ receptor and serotonin transporter (SERT) availability, showing absence of depressive symptoms 2 weeks after RSD. We combined behavioral tests and positron emission tomography (PET) with [¹¹C]raclopride and [¹¹C]DASB to explore the changes in dopamine D₂/D₃ receptor and serotonin transporter (SERT) availability, respectively. Male rats submitted to RSD showed increased peripheral corticosterone levels, decreased body weight and anhedonia, as measured with the sucrose preference test, 1 day after RSD, confirming depressive-like symptoms. These depressive-like symptoms were no longer present 2 weeks after RSD. Rats that recovered from depressive-like symptoms showed decreased D₂/D₃ receptor binding in the caudate putamen and increased SERT availability in the brainstem, insular cortex, midbrain and thalamus, compared to control non-stressed animals. Our study shows that remission of depressive-like symptoms does not just “normalize” monoaminergic transmission, as changes in dopaminergic and serotonergic neurotransmission linger in several brain regions even after depressive-like symptoms have already resolved. These results provide new insights into the brain changes associated to remission in the RSD-induced depression model in rats.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106727"},"PeriodicalIF":5.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neonatal hypoxia-ischemia alters the events governing the hippocampal critical period of postnatal synaptic plasticity leading to deficits in working memory in mice","authors":"Pritika Parmar ,&nbsp;Harisa Spahic ,&nbsp;Charles Lechner ,&nbsp;Mark St. Pierre ,&nbsp;Katherine Carlin ,&nbsp;Michael Nugent ,&nbsp;Raul Chavez-Valdez","doi":"10.1016/j.nbd.2024.106722","DOIUrl":"10.1016/j.nbd.2024.106722","url":null,"abstract":"<div><div>Postnatal critical periods of synaptic plasticity (CPsp) are characterized by profound neural network refinement, which is shaped by synaptic activity and sculpted by maturation of the GABAergic network. Even after therapeutic hypothermia (TH), neonatal hypoxia-ischemia (HI) impairs two triggers for the initiation of the CPsp in the hippocampus: i) PSA-NCAM developmental decline and ii) parvalbumin (PV) + interneuron (IN) maturation. Thus, we investigated whether neonatal HI despite TH disturbs other events governing the onset, consolidation and closure of the postnatal CPsp in the hippocampus. We induced cerebral HI in P10 C57BL6 mice with right carotid ligation and 45 m of hypoxia (FiO₂ = 0.08), followed by normothermia (36 °C, NT) or TH (31 °C) for 4 h with anesthesia-exposed shams as controls. ELISA, immunoblotting and immunohistochemistry were performed at 24 h (P11), 5 days (P15), 8 days (P18) and 30 days (P40) after HI injury. We specifically assessed: i) BDNF levels and TrkB activation, controlling the CPsp, ii) Otx2 and NPTX2 immunoreactivity (IR), engaging CPsp onset and iii) NogoR1, Lynx1 IR, PNN formation and myelination (MBP) mediating CPsp closure. Pups aged to P40 also received a battery of tests assessing working memory. Here, we documented deficits in hippocampal BDNF levels and TrkB activation at P18 in response to neonatal HI even with TH. Neonatal HI impaired in the CA1 the developmental increase in PV, Otx2, and NPTX2 between P11 and P18, the colocalization of Otx2 and PV at P18 and P40, the accumulation of NPTX2 in PV⁺ dendrites at P18 and P40, and the expression of NogoR at P40. Furthermore, neonatal HI decreased BDNF and impaired PNN development and myelination (MBP) at P40. Most of these abnormalities were insensitive to TH and correlated with memory deficits. Neonatal HI appears to disrupt many of the molecular and structural events initiating and consolidating the postnatal hippocampal CPsp, perhaps due to the early and delayed deficits in TrkB activation leading to memory deficits.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106722"},"PeriodicalIF":5.1,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sphingosine 1-phosphate receptor subtype 1 (S1P1) activity in the course of Alzheimer's disease","authors":"Jonatan Martínez-Gardeazabal ,&nbsp;Gorka Pereira-Castelo ,&nbsp;Marta Moreno-Rodríguez ,&nbsp;Alberto Llorente-Ovejero ,&nbsp;Manuel Fernández ,&nbsp;Iván Fernández-Vega ,&nbsp;Iván Manuel ,&nbsp;Rafael Rodríguez-Puertas","doi":"10.1016/j.nbd.2024.106713","DOIUrl":"10.1016/j.nbd.2024.106713","url":null,"abstract":"<div><div>Some specific lipid molecules in the brain act as signaling molecules, neurotransmitters, or neuromodulators, by binding to specific G protein-coupled receptors (GPCR) for neurolipids. One such receptor, sphingosine 1-phosphate receptor subtype 1 (S1P₁), is coupled to G_i/o proteins and is involved in cell proliferation, growth, and neuroprotection. S1P₁ constitutes an interesting target for neurodegenerative diseases like multiple sclerosis and Alzheimer's disease (AD), in which changes in the sphingolipid metabolism have been observed. This study analyzes S1P₁ receptor-mediated activity in healthy brains and during AD progression using <em>postmortem</em> samples from controls and patients at different Braak's stages. Additionally, the distribution of S1P₁ receptor activity in human brains is compared to that in commonly used rodent models, rats and mice, through functional autoradiography, measuring [³⁵S]GTPγS binding stimulated by the S1P₁ receptor selective agonist CYM-5442 to obtain the distribution of functional activity of S1P₁ receptors.</div><div>S1P₁ receptor-mediated activity, along with that of the cannabinoid CB₁ receptor, is one of the highest recorded for any GPCR in many gray matter areas of the brain, reaching maximum values in the cerebellar cortex, specific areas of the hippocampus and the basal forebrain. S1P₁ signaling is crucial in areas that regulate learning, memory, motor control, and nociception, such as the basal forebrain and basal ganglia. In AD, S1P₁ receptor activity is increased in the inner layers of the frontal cortex and underlying cortical white matter at early stages, but decreases in the hippocampus in advanced stages, indicating ongoing brain impairment. Importantly, we identified significant correlations between S1P₁ receptor activity and Braak stages, suggesting that S1P₁ receptor dysfunction is associated to disease progression, particularly in memory-related regions. The S1P signaling <em>via</em> S1P₁ receptor is a promising neurological target due to its role in key neurophysiological functions and its potential to modify the progression of neurodegenerative diseases. Finally, rats are suggested as a preferred experimental model for studying S1P₁ receptor-mediated responses in the human brain.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106713"},"PeriodicalIF":5.1,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senolytic therapy preserves blood-brain barrier integrity and promotes microglia homeostasis in a tauopathy model","authors":"Minmin Yao ,&nbsp;Zhiliang Wei ,&nbsp;Jonathan Scharff Nielsen ,&nbsp;Yuxiao Ouyang ,&nbsp;Aaron Kakazu ,&nbsp;Haitong Wang ,&nbsp;Lida Du ,&nbsp;Ruoxuan Li ,&nbsp;Tiffany Chu ,&nbsp;Susanna Scafidi ,&nbsp;Hanzhang Lu ,&nbsp;Manisha Aggarwal ,&nbsp;Wenzhen Duan","doi":"10.1016/j.nbd.2024.106711","DOIUrl":"10.1016/j.nbd.2024.106711","url":null,"abstract":"<div><div>Cellular senescence, characterized by expressing the cell cycle inhibitory proteins, is evident in driving age-related diseases. Senescent cells play a crucial role in the initiation and progression of tau-mediated pathology, suggesting that targeting cell senescence offers a therapeutic potential for treating tauopathy associated diseases. This study focuses on identifying non-invasive biomarkers and validating their responses to a well-characterized senolytic therapy combining dasatinib and quercetin (D + Q), in a widely used tauopathy mouse model, PS19. We employed human-translatable MRI measures, including water extraction with phase-contrast arterial spin tagging (WEPCAST) MRI, T2 relaxation under spin tagging (TRUST), longitudinally assessed brain physiology and high-resolution structural MRI evaluated the brain regional volumes in PS19 mice. Our data reveal increased BBB permeability, decreased oxygen extraction fraction, and brain atrophy in 9-month-old PS19 mice compared to their littermate controls. (D + Q) treatment effectively preserves BBB integrity, rescues cerebral oxygen hypometabolism, attenuates brain atrophy, and alleviates tau hyperphosphorylation in PS19 mice. Mechanistically, D + Q treatment induces a shift of microglia from a disease-associated to a homeostatic state, reducing a senescence-like microglial phenotype marked by increased p16/Ink4a. D + Q-treated PS19 mice exhibit enhanced cue-associated cognitive performance in the tracing fear conditioning test compared to the vehicle-treated littermates, implying improved cognitive function by D + Q treatment. Our results pave the way for application of senolytic treatment as well as these noninvasive MRI biomarkers in clinical trials in tauopathy associated neurological disorders.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106711"},"PeriodicalIF":5.1,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nigrostriatal tract defects in mice with aromatic l-amino acid decarboxylase deficiency","authors":"Ni-Chung Lee ,&nbsp;Pei-Chun Hsu ,&nbsp;Yu-Han Liu ,&nbsp;Hao-Chun Wang ,&nbsp;Tsu-I Chen ,&nbsp;Yin-Hsiu Chien ,&nbsp;Wuh-Liang Hwu","doi":"10.1016/j.nbd.2024.106707","DOIUrl":"10.1016/j.nbd.2024.106707","url":null,"abstract":"<div><div>The development of the nigrostriatal dopaminergic (DA) pathway in the brain involves many transcriptional and chemotactic molecules, and a deficiency of these molecules can cause nigrostriatal tract defects. However, the role of the end product, dopamine, in nigrostriatal pathway development has not been described. In the present study, we analyzed a mouse model of congenital dopamine and serotonin deficiency, namely, the aromatic <span>l</span>-amino acid decarboxylase (AADC) deficiency (<em>Ddc</em>^KI) mouse model. We found via tyrosine hydroxylase (TH) immunofluorescence staining that the number of DA fibers in the stratum of 14-day-old <em>Ddc</em>^KI mice decreased. In TH-stained cleared whole brains of <em>Ddc</em>^KI mice, the numbers of DA neurons in the substantia nigra (SN) and the number of DA nerve bundles leaving the SN were both normal. However, we found that the nigrostriatal bundles in <em>Ddc</em>^KI mice were dispersed, taking aberrant routes to the striatum and spreading over a wide area. The total volume occupied by the nigrostriatal tract was increased, and the fraction of TH staining in the tract was decreased in <em>Ddc</em>^KI mice. Single-nucleus RNA sequencing analysis for mice 0, 7, and 14 days of age, revealed delayed axonogenesis and synapse formation in the striatum of <em>Ddc</em>^KI mice. The CellChat program inferred less cell–cell communication between striatal D1/D2 neurons but increased cell–cell communication involving neural precursors in <em>Ddc</em>^KI mice. Therefore, a congenital deficiency in dopamine affects nigrostriatal axon extension and striatal innervation. These nigrostriatal tract defects may limit the treatment efficacy for patients with TH or AADC deficiency.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106707"},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A timeline study on vascular co-morbidity induced cerebral endothelial dysfunction assessed by perfusion MRI","authors":"Bram Callewaert ,&nbsp;Willy Gsell ,&nbsp;Marleen Lox ,&nbsp;Uwe Himmelreich ,&nbsp;Elizabeth A.V. Jones","doi":"10.1016/j.nbd.2024.106709","DOIUrl":"10.1016/j.nbd.2024.106709","url":null,"abstract":"<div><div>Endothelial dysfunction is considered a key element in the early pathogenesis of neurodegenerative disorders. Dysfunction of the cerebral endothelial cells can result in dysregulation of cerebral perfusion and disruption of the Blood Brain Barrier (BBB), leading to brain damage, neurodegeneration and cognitive decline. It has been shown that the presence of modifiable risk factors exacerbates endothelial dysfunction. This study primarily aimed to identify which among various perfusion MRI methodologies could be effectively utilized to non-invasively identify early pathological alterations as a result of endothelial dysfunction. We compared these perfusion MRI measurements to invasive immunohistochemistry to detect early pathological alterations in the cerebral vasculature of a rat model of multiple cardiovascular co-morbidities (the ZSF1 Obese rat) at several stages of the cerebrovascular pathology. We observed cerebral hyperperfusion, expressed by increased Cerebral Blood Flow (CBF) and increased BBB permeability in the ZSF1 Obese rats, at an early stage of disease development. The increase in CBF observed with Arterial Spin Labeling (ASL) was lost during later stages of disease progression. These findings are in line with recent clinical findings in early stages of Alzheimer's disease (AD), that also show early increases in CBF.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106709"},"PeriodicalIF":5.1,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiomics approach discloses lipids and metabolites profiles associated to Parkinson's disease stages and applied therapies","authors":"Federica Carrillo ,&nbsp;Nicole Piera Palomba ,&nbsp;Marco Ghirimoldi ,&nbsp;Camilla Didò ,&nbsp;Giorgio Fortunato ,&nbsp;Shahzaib Khoso ,&nbsp;Tiziana Giloni ,&nbsp;Marco Santilli ,&nbsp;Tommaso Bocci ,&nbsp;Alberto Priori ,&nbsp;Sara Pietracupa ,&nbsp;Nicola Modugno ,&nbsp;Elettra Barberis ,&nbsp;Marcello Manfredi ,&nbsp;Paola Signorelli ,&nbsp;Teresa Esposito","doi":"10.1016/j.nbd.2024.106698","DOIUrl":"10.1016/j.nbd.2024.106698","url":null,"abstract":"<div><div>Profiling circulating lipids and metabolites in Parkinson's disease (PD) patients could be useful not only to highlight new pathways affected in PD condition but also to identify sensitive and effective biomarkers for early disease detection and potentially effective therapeutic interventions. In this study we adopted an untargeted omics approach in three groups of patients (No L-Dopa, L-Dopa and DBS) to disclose whether long-term levodopa treatment with or without deep brain stimulation (DBS) could reflect a characteristic lipidomic and metabolomic signature at circulating level. Our findings disclosed a wide up regulation of the majority of differentially regulated lipid species that increase with disease progression and severity. We found a relevant modulation of triacylglycerols and acyl-carnitines, together with an altered profile in adiponectin and leptin, that can differentiate the DBS treated group from the others PD patients. We found a highly significant increase of exosyl ceramides (Hex2Cer) and sphingoid bases (SPB) in PD patients mainly in DBS group (<em>p</em> &lt; 0.0001), which also resulted in a highly accurate diagnostic performance. At metabolomic level, we found a wide dysregulation of pathways involved in the biosynthesis and metabolism of several amino acids. The most interesting finding was the identification of a specific modulation of L-glutamic acid in the three groups of patients. L-glutamate levels increased slightly in No L-Dopa and highly in L-Dopa patients while decreased in DBS, suggesting that DBS therapy might have a beneficial effect on the glutamatergic cascade. All together, these data provide novel insights into the molecular and metabolic alterations underlying PD therapy and might be relevant for PD prediction, diagnosis and treatment.</div></div>","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"202 ","pages":"Article 106698"},"PeriodicalIF":5.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Special issue on “A focus on brain–body communication in understanding the neurobiology of diseases”","authors":"Kenji Hashimoto ,&nbsp;Yan Wei ,&nbsp;Chun Yang","doi":"10.1016/j.nbd.2024.106666","DOIUrl":"10.1016/j.nbd.2024.106666","url":null,"abstract":"","PeriodicalId":19097,"journal":{"name":"Neurobiology of Disease","volume":"201 ","pages":"Article 106666"},"PeriodicalIF":5.1,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142254701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}