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BIOS-02. RECAPITULATE TUMOR DIVERSION AND SPATIAL PATTERNING IN GLIOBLASTOMA BACKGROUND

Neuro-Oncology 2023年第SUPPLEMENT_5期25卷 v20-v20页

作者： Lo, Wei-Lun Khoa, Hoang Dang Ta Chuang, Jian-Ying Division of Neurosurgery Shuang-Ho Hospital New Taipei City New Taipei Taiwan (Republic of China) PhD Program for Cancer Molecular Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University and Academia Sinica Taipei Taipei Taiwan (Republic of China) International Master Program in Medical Neuroscience Taipei Medical University Taipei Taiwan (Republic of China)

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MiR34 contributes to spinal muscular atrophy and AAV9-mediated delivery of MiR34a ameliorates the motor deficits in SMA mice

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Molecular therapy. Nucleic acids 2023年 32卷 144-160页

作者： Tai-Heng Chen Shih-Hsin Chang Yu-Fu Wu Ya-Ping Yen Fang-Yu Hsu Yen-Chung Chen Yang Ming Ho-Chiang Hsu Yi-Ching Su Sheng-Tang Wong Jui-Hung Hung Shih-Hwa Chiou Yuh-Jyh Jong Jun-An Chen PhD Program in Translational Medicine Kaohsiung Medical University Kaohsiung 80708 and Academia Sinica Taipei 11529 Taiwan. Institute of Molecular Biology Academia Sinica Taipei 11529 Taiwan. Department of Pediatrics Kaohsiung Medical University Kaohsiung 80708 Taiwan. School of Post-Baccalaureate Medicine Kaohsiung Medical University Kaohsiung 80708 Taiwan. Neuroscience Program of Academia Sinica Academia Sinica Taipei 11529 Taiwan. Department of Computer Science National Yang Ming Chiao Tung University Hsinchu 30093 Taiwan. Institute of Pharmacology School of Medicine National Yang Ming Chiao Tung University Taipei 11221 Taiwan. Innovative Cellular Therapy Center Department of Medical Research Taipei Veterans General Hospital Taipei 11217 Taiwan. Department of Laboratory Medicine Kaohsiung Medical University Kaohsiung 80708 Taiwan. Translational Research Center of Neuromuscular Diseases Kaohsiung Medical University Hospital Kaohsiung Medical University Kaohsiung 80708 Taiwan. Graduate Institute of Clinical Medicine College of Medicine Kaohsiung Medical University Kaohsiung 80708 Taiwan. Drug Development and Value Creation Research Center Kaohsiung Medical University Kaohsiung 80708 Taiwan. Department of Biological Science and Technology National Yang Ming Chiao Tung University Hsinchu 30093 Taiwan.

Spinal muscular atrophy (SMA) is a neurodegenerative disease characterized by the selective loss of spinal motor neurons (MNs) and concomitant muscle weakness. Mutation of is known to cause SMA, and restoring SMN protein levels via antisense oligonucleotide treatment is effective for ameliorating symptoms. However, this approach is hindered by exorbitant costs, invasive procedures, and poor treatment responses of some patients. Here, we seek to circumvent these hurdles by identifying reliable biomarkers that could predict treatment efficacy. We uncovered that MiR34 exhibits consistent downregulation during SMA progression in both human and rodent contexts. Importantly, family-knockout mice display axon swelling and reduced neuromuscular junction (NMJ) endplates, recapitulating SMA pathology. Introducing MiR34a via scAAV9 improved the motor ability of SMNΔ7 mice, possibly by restoring NMJ endplate size. Finally, we observed a consistent decreasing trend in MiR34 family expression in the cerebrospinal fluid (CSF) of type I SMA patients during the loading phase of nusinersen treatment. Baseline CSF MiR34 levels before nusinersen injection proved predictive of patient motor skills 1 year later. Thus, we propose that MiR34 may serve as a biomarker of SMA since it is associated with the pathology and can help evaluate the therapeutic effects of nusinersen.

关键词： ASO MT: Non-coding RNAs MiR34 SMA biomarker microRNA nusinersen spinal muscular atrophy

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Molecular hallmarks of hydrocephalus

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Science translational medicine 2025年第801期17卷 eadq1810页

作者： Andrew T Hale Blake Zhou Arjun Rajan Phan Q Duy Mubeen Goolam Seth L Alper Maria K Lehtinen Madeline A Lancaster Ryann M Fame Kristopher T Kahle Department of Neurosurgery University of Alabama at Birmingham Birmingham AL 35233 USA. Department of Human Biology and Neuroscience Institute University of Cape Town Cape Town 7925 South Africa. Neurosciences Graduate Program Stanford University Stanford CA 94305 USA. Developmental Biology Graduate Program Stanford University Stanford CA 94305 USA. Department of Neurosurgery University of Virginia School of Medicine Charlottesville VA 22903 USA. Division of Nephrology and Vascular Biology Research Center Beth Israel Deaconess Medical Center Boston MA 02215 USA. Department of Medicine Harvard Medical School Boston MA 02115 USA. Broad Institute of MIT and Harvard Cambridge MA 02142 USA. Department of Pathology Boston Children's Hospital and Harvard Medical School Boston MA 02115 USA. Medical Research Council Laboratory for Molecular Biology University of Cambridge Cambridge CB2 0QH UK. Department of Neurosurgery Stanford University School of Medicine Palo Alto CA 94304 USA. Department of Neurosurgery Harvard Medical School and Massachusetts General Hospital Boston MA 02114 USA. Division of Genetics and Genomics and Manton Center for Orphan Disease Research Boston Children's Hospital Boston MA 02115 USA. Harvard PhD Program in Neuroscience (PiN) Harvard University Cambridge MA 02115 USA.

Hydrocephalus (HC) is a failure of brain and cerebrospinal fluid (CSF) homeostasis often associated with dilation of the CSF-filled ventricles (ventriculomegaly). Hallmarks of HC include aberrant CSF dynamics, neural stem cell dysfunction resulting in impaired neurogenesis and corticogenesis, biomechanical instability at the brain-CSF interface, and disrupted synaptogenesis and neural circuitry. Pleiotropic mechanisms, including genetic and environmental insults to the brain, contribute to neurodevelopmental comorbidities. Hypothesis generation from genome-wide, single-cell multi-omic analyses coupled to experimental validation using induced pluripotent stem cell-derived cerebral organoids will refine molecular classification of HC subtypes and may lead to precision-based surgical and pharmacologic treatments.

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Author Correction: Low-intensity pulsed ultrasound stimulation (LIPUS) modulates microglial activation following intracortical microelectrode implantation

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Nature communications 2024年第1期15卷 7618页

作者： Fan Li Jazlyn Gallego Natasha N Tirko Jenna Greaser Derek Bashe Rudra Patel Eric Shaker Grace E Van Valkenburg Alanoud S Alsubhi Steven Wellman Vanshika Singh Camila Garcia Padilla Kyle W Gheres John I Broussard Roger Bagwell Maureen Mulvihill Takashi D Y Kozai Department of Bioengineering University of Pittsburgh Pittsburgh PA USA. Center for Neural Basis of Cognition Pittsburgh PA USA. Computational Modeling and Simulation PhD Program University of Pittsburgh Pittsburgh PA USA. Department of Biochemistry and Molecular Biology Pennsylvania State University University Park PA USA. Actuated Medical Bellefonte PA USA. Washington University in St. Louis St. Louis MO USA. Department of Neuroscience University of Pittsburgh Pittsburgh PA USA. Columbia University New York NY USA. Department of Bioengineering University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. Center for Neural Basis of Cognition Pittsburgh PA USA. TK.Kozai@pitt.edu. Center for Neuroscience University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. McGowan Institute of Regenerative Medicine University of Pittsburgh Pittsburgh PA USA. TK.Kozai@pitt.edu. NeuroTech Center University of Pittsburgh Brain Institute Pittsburgh PA USA. TK.Kozai@pitt.edu.

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腺苷受体是调节大脑内侧前额叶皮质星形胶质细胞大麻素1型(CB1)受体对突触可塑性作用的开关

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神经损伤与功能重建 2024年第4期19卷 250页

作者： Joana Gon?alves-Ribeiro Oksana K Savchak Sara Costa-Pinto Joana I Gomes Rafael Rivas-Santisteban Alejandro Lillo Javier Sánchez Romero Ana M Sebasti?o Marta Navarrete Gemma Navarro Rafael Franco Sandra H Vaz Instituto de Farmacologia e Neurociencias Faculdade de MedicinaUniversidade de Lisboa Instituto de Medicina Molecular Joao Lobo Antunes Faculdade de MedicinaUniversidade de Lisboa Department of Biochemistry and Physiology School of Pharmacy and Food ScienceUniversitat de Barcelona CiberNed Network Center for Neurodegenerative DiseasesNational Spanish Health Institute Carlos Ⅲ Instituto Cajal CSIC PhD Program in Neuroscience Universidad Autonoma de Madrid-Instituto Cajal Institut de Neurociencies Universitat de Barcelona Molecular Neurobiology Laboratory Department of Biochemistry and Molecular BiomedicineFaculty of Biology School of Chemistry Universitat de Barcelona

内侧前额叶皮质（mPFC）参与诸如工作记忆等认知功能。星形胶质细胞大麻素1型受体（CB1R）诱导细胞质内钙离子(Ca2+)浓度变化,对神经元功能产生影响。mPFC的星形胶质细胞也表达腺苷A1和A2A受体(A1R,A2AR),但目前尚不清楚这些细胞中的CB1... 详细信息

内侧前额叶皮质（mPFC）参与诸如工作记忆等认知功能。星形胶质细胞大麻素1型受体（CB1R）诱导细胞质内钙离子(Ca2+)浓度变化,对神经元功能产生影响。mPFC的星形胶质细胞也表达腺苷A1和A2A受体(A1R,A2AR),但目前尚不清楚这些细胞中的CB1R与腺苷受体之间的交流。我们在这里展示,通过CB1R-A2AR或CB1R-A1R异源二聚体,星形胶质细胞Ca2+信号传递发生了进一步的调节,最终影响mPFC突触可塑性。当A1R和A2AR被激活时,CB1R介导的Ca2+瞬变出现增加或减少,揭示了腺苷受体可能是星形胶质细胞CB1R的调节器。CB1R的激活导致mPFC的长时程增强（LTP）增强,受A1R控制,但不受A2AR控制。值得注意的是,在IP3R2KO小鼠中,由于没有显示出星形胶质细胞Ca2+水平升高,CB1R的激活减少了LTP,这种效果不受A1R或A2AR的调节。本研究表明,CB1R在mPFC LTP上具有稳态作用,受到A1R的控制,可能是由于这些受体在星形胶质细胞中的交流,最终改变了CB1R Ca2+信号传递。

关键词： CB1受体腺苷受体星形胶质细胞内侧前额叶皮质突触可塑性

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Correction : IL-1R1 signaling in TBI: assessing chronic impacts and neuroinflammatory dynamics in a mouse model of mild closed-head injury

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Journal of neuroinflammation 2023年第1期20卷 287页

作者： Jonathan C Vincent Colleen N Garnett James B Watson Emma K Higgins Teresa Macheda Lydia Sanders Kelly N Roberts Ryan K Shahidehpour Eric M Blalock Ning Quan Adam D Bachstetter Department of Neuroscience University of Kentucky 741 S. Limestone St. Lexington KY 40536 USA. Spinal Cord and Brain Injury Research Center University of Kentucky Lexington KY USA. Sanders‑Brown Center on Aging University of Kentucky Lexington KY USA. MD/PhD Program University of Kentucky Lexington KY USA. Department of Cell Developmental and Integrative Biology University of Alabama at Birmingham Birmingham AL USA. Department of Pharmacology and Nutritional Sciences University of Kentucky Lexington KY USA. Department of Biomedical Science Charles E. Schmidt College of Medicine and Brain Institute Florida Atlantic University Jupiter FL USA. Department of Neuroscience University of Kentucky 741 S. Limestone St. Lexington KY 40536 USA. adam.bachstetter@uky.edu. Spinal Cord and Brain Injury Research Center University of Kentucky Lexington KY USA. adam.bachstetter@uky.edu. Sanders‑Brown Center on Aging University of Kentucky Lexington KY USA. adam.bachstetter@uky.edu.

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Pericyte-like spreading by disseminated cancer cells activates YAP and MRTF for metastatic colonization (vol 20, pg 966, 2018)

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NATURE CELL biology 2019年第3期21卷 408-408页

作者： Er, Ekrem Emrah Valiente, Manuel Ganesh, Karuna Zou, Yilong Agrawal, Saloni Hu, Jing Griscom, Bailey Rosenblum, Marc Boire, Adrienne Brogi, Edi Giancotti, Filippo G. Schachner, Melitta Malladi, Srinivas Massague, Joan Cancer Biology and Genetics Program Memorial Sloan Kettering Cancer Center New York USA Brain Metastasis Group Spanish National Cancer Research Center (CNIO) Madrid Spain Department of Medicine Memorial Sloan Kettering Cancer Center New York USA Department of Pathology Memorial Sloan Kettering Cancer Center New York USA Department of Neurology Memorial Sloan Kettering Cancer Center New York USA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer Center New York USA Department of Cancer Biology and David E. Koch Center for Applied Research of Genitourinary Cancers The University of Texas MD Anderson Cancer Center Houston USA Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience Rutgers University Piscataway USA Center for Neuroscience Shantou University Medical College Shantou China Department of Pathology The University of Texas Southwestern Medical Center Dallas USA

In the version of this Article originally published, the authors inadvertently included the term 'pericytic mimicry' in relation to ref. 54. This has now been corrected by inserting an additional reference at position 51 and amending the text in the Discussion relating to 'pericytic mimicry', ref. 54 and pericyte-like spreading. The original refs 51-70 have also been renumbered. Furthermore, Fig. 8l has been amended to remove the term 'pericyte mimicry' that the authors had included inadvertently during figure preparation. These corrections have been made in the online versions of the Article.

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Consensus guidelines for assessing eligibility of pathogenic DNA variants for antisense oligonucleotide treatments

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American Journal of Human Genetics 2025年第5期112卷 975-983页

作者： Cheerie, David Meserve, Margaret M. Beijer, Danique Kaiwar, Charu Newton, Logan Taylor Tavares, Ana Lisa Verran, Aubrie Soucy Sherrill, Emma Leonard, Stefanie Sanders, Stephan J. Blake, Emily Elkhateeb, Nour Gandhi, Aastha Liang, Nicole S.Y. Morgan, Jack T. Verwillow, Anna Verheijen, Jan Giles, Andrew Williams, Sean Chopra, Maya Croft, Laura Dafsari, Hormos Salimi Davidson, Alice E. Friedman, Jennifer Gregor, Anne Haque, Bushra Lechner, Rosan Montgomery, Kylie-Ann Ryten, Mina Schober, Emil Siegel, Gabriele Sullivan, Patricia J. Whittle, Ella F. Zardetto, Bianca Yu, Timothy W. Synofzik, Matthis Aartsma-Rus, Annemieke Costain, Gregory Lauffer, Marlen C. Program in Genetics & Genome Biology SickKids Research Institute Toronto M5G 0A4 ON Canada Department of Molecular Genetics University of Toronto Toronto M5S 1A8 ON Canada Division of Genetics and Genomics Boston Children's Hospital Boston 02115 MA United States Division of Translational Genomics of Neurodegenerative Diseases Hertie Institute for Clinical Brain Research and Center of Neurology University of Tübingen Tübingen 72076 Germany German Center of Neurodegenerative Diseases (DZNE) Tübingen 72076 Germany Clinical Molecular Geneticist Department of Pathology and Laboratory Medicine Precision Diagnostics Laboratory Children's Hospital Colorado Aurora 80045 CO United States Genomics England London E14 5AB United Kingdom Department of Clinical Genetics Cambridge University Hospitals NHS Foundation Trust Cambridge Cambridgeshire CB2 0QQ United Kingdom N=1 Collaborative 7 Carole Place Somerville 02143 MA United States Institute of Developmental and Regenerative Medicine Department of Pediatrics University of Oxford Oxford OX3 7TY United Kingdom Department of Psychiatry and Behavioral Sciences UCSF Weill Institute for Neurosciences University of California San Francisco San Francisco 94158 CA United States New York Genome Center New York 10013 NY United States Department of Quantitative Health Sciences Mayo Clinic Rochester 55902 MN United States Division of Clinical & Metabolic Genetics Hospital for Sick Children Toronto M5G 1X8 ON Canada Department of Genetic Counselling Hospital for Sick Children Toronto M5G 1X8 ON Canada Dutch Center for RNA Therapeutics Department of Human Genetics Leiden University Medical Center Leiden 2333 ZA Netherlands Center for Genomic Medicine Massachusetts General Hospital 55 Fruit Street Boston 02114 MA United States Department of Pathology University of Utah School of Medicine Salt Lake City 84112 UT United States ARUP Laboratories Salt Lake City 84108 UT United States Ambry Genetics 1 E

Of the around 7,000 known rare diseases worldwide, disease-modifying treatments are available for fewer than 5%, leaving millions of individuals without specialized therapeutic strategies. In recent years, antisense oligonucleotides (ASOs) have shown promise as individualized genetic interventions for rare genetic diseases. However, there is currently no consensus on which disease-causing DNA variants are suitable candidates for this type of genetic therapy. The patient identification working group of the N=1 collaborative (N1C), alongside an international group of volunteer assessors, has developed and piloted consensus guidelines for assessing the eligibility of pathogenic DNA variants for ASO treatments. We herein present the N1C VARIANT (variant assessments toward eligibility for antisense oligonucleotide treatment) guidelines, including the guiding scientific principles and our approach to consensus building. Pathogenic, disease-causing variants can be assessed for the three currently best-established ASO treatment approaches: splice correction, exon skipping, and downregulation of RNA transcripts. A genetic variant is classified as “eligible,” “likely eligible,” “unlikely eligible,” or “not eligible” in relation to the different approaches or as “unable to assess.” We also review key considerations related to assessing the upregulation of transcripts from the wild-type allele, an emerging ASO therapeutic strategy. We provide additional tools and training materials to enable clinicians and researchers to use these guidelines for their eligibility assessments. With this initial edition of our N1C VARIANT guidelines, we provide the rare genetic disease community with guidance on how to identify suitable candidates for variant-specific ASO-based therapies and the possibility of integrating such assessments into routine clinical practice. © 2025 The Authors

关键词： antisense oligonucleotides consensus guidelines individualized genetic therapies personalized medicine rare genetic diseases

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The ADAMTs family protease MIG-17 orchestrates synaptic connections in *** during postnatal development

The ADAMTs family protease MIG-17 orchestrates synaptic conn...

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第五届中国秀丽线虫大会

作者： Tingting Ji Kai Wang Jichang Huang Mengqing Wang Xiaohua Dong Yanjun Shi Xumin Zhang Zhiyong Shao Daniel A.Colón-Ramos State Key Laboratory of Medical Neurobiology Collaborative Innovation Center for Brain Science and the Institutes of Brain ScienceDepartment of NeurologyZhongshan HospitalFudan University State Key Laboratory of Genetic Engineering Department of BiochemistrySchool of Life SciencesFudan University Program in Cellular Neuroscience Neurodegenerationand RepairDepartment of Cell Biology and Department of NeuroscienceYale University School of Medicine

Synapses are essential for the neuronal *** connections are formed during early developmental stage with remarkable specificity both at the target cell and subcellular location *** establishment,most of those connections are maintained even for life *** the spatial specificity of synaptic connection is maintained during growth when the volume is dramatic increased is largely unknown.

关键词： MIG The ADAMTs family protease MIG-17 orchestrates synaptic connections in C.elegans during postnatal development

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P–074 Chromatin Maturity Index (CMI) in unfixed and live spermatozoa and Aniline Blue (AB) stained as an additional evaluation parameter in idiopathic male infertility

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Human Reproduction 2021年第SUPPLEMENT_1期36卷

作者： Notari, T Piscopo, M Bosco, L Pecoraro, S Serra, N Ricciardi, D Capra, G Montano, L Check Up - Day Surgery Polydiagnostic Centre Salerno- Italy. Check Up Research Unit Salerno Italy University of Naples “Federico II” Department of Biology Napoli Italy University of Palermo Department of Biomedicine- Neuroscience and Advanced Diagnostics Bi.N.D- Section of Biology and Genetics- Palermo- Italy IRCCS Neuromed “Malzoni Clinic” Department of Uro-Andrology- Avellino Italy University of Naples “Federico II” Department of Public Health Napoli Italy “Ricciardi” Diagnostic Centre Seminology Lab Pollena Trocchia- Napoli Italy University of Palermo Department of Sciences for Health Promotion and Mother-Child Care ‘G. D’Alessandro’ PROSAMI- Palermo Italy Local Health Authority ASL-Salerno.. Andrology Unit and Service of Lifestyle Medicine in UroAndrology- Coordination Unit of the network for Environmental and Reproductive Health EcoFoodFertility project- “Oliveto Citra Hospital”- Salerno. PhD Program

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