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Author Correction: Progressive plasticity during colorectal cancer metastasis

Nature 2025年第8047期637卷 E28页

作者： Andrew Moorman Elizabeth K Benitez Francesco Cambuli Qingwen Jiang Ahmed Mahmoud Melissa Lumish Saskia Hartner Sasha Balkaran Jonathan Bermeo Simran Asawa Canan Firat Asha Saxena Fan Wu Anisha Luthra Cassandra Burdziak Yubin Xie Valeria Sgambati Kathleen Luckett Yanyun Li Zhifan Yi Ignas Masilionis Kevin Soares Emmanouil Pappou Rona Yaeger T Peter Kingham William Jarnagin Philip B Paty Martin R Weiser Linas Mazutis Michael D'Angelica Jinru Shia Julio Garcia-Aguilar Tal Nawy Travis J Hollmann Ronan Chaligné Francisco Sanchez-Vega Roshan Sharma Dana Pe'er Karuna Ganesh Computational and Systems Biology Program Memorial Sloan Kettering Cancer Center New York NY USA. Molecular Pharmacology Program Memorial Sloan Kettering Cancer Center New York NY USA. Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program New York NY USA. New York Genome Center New York NY USA. Pharmacology Program Weill Cornell Graduate School New York NY USA. Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Case Western Reserve University Cleveland OH USA. Department of Pathology and Laboratory Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Department of Surgery Memorial Sloan Kettering Cancer Center New York NY USA. Tri-Institutional PhD Program in Computational Biology and Medicine New York NY USA. Bristol Myers Squibb Princeton NJ USA. Computational and Systems Biology Program Memorial Sloan Kettering Cancer Center New York NY USA. peerd@***. Howard Hughes Medical Institute Chevy Chase MD USA. peerd@***. Molecular Pharmacology Program Memorial Sloan Kettering Cancer Center New York NY USA. ganeshk@***. Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. ganeshk@***.

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Outdoor Air Pollution Relates to Amygdala Subregion Volume and Apportionment in Early Adolescence

Biological Psychiatry Global Open Science

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Biological Psychiatry Global Open Science 2025年

作者： Jessica Morrel L. Nate Overholtzer Kirthana Sukumaran Devyn L. Cotter Carlos Cardenas-Iniguez J. Michael Tyszka Joel Schwartz Daniel A. Hackman Jiu-Chiuan Chen Megan M. Herting Department of Population and Public Health Sciences Keck School of Medicine University of Southern California Los Angeles CA USA Neuroscience Graduate Program University of Southern California Los Angeles CA USA USC-Caltech MD-PhD Program Los Angeles CA USA Division of the Humanities and Social Sciences California Institute of Technology Pasadena CA USA Department of Environmental Health Harvard T.H. Chan School of Public Health Boston MA USA USC Suzanne Dworak-Peck School of Social Work University of Southern California Los Angeles CA USA Department of Neurology Keck School of Medicine of University of Southern California Los Angeles CA USA

Background Outdoor air pollution exposure is associated with structural and functional brain differences, and an increased risk for psychopathology. Although the neural mechanisms remain unclear, air pollutants may impact mental health by altering brain regions implicated in psychopathology, such as the amygdala. Here, we examine the association between ambient air pollution exposure and amygdala subregion volumes in 9–10-year-olds. Methods Cross-sectional data from 4,473 (55.4% male) Adolescent Brain Cognitive Development SM (ABCD) Study® participants were leveraged. Air pollution exposure was estimated based on each participant’s primary residential address. Using the CIT168 atlas, we quantified total amygdala and 9 subregion volumes from T1- and T2-weighted images. We investigated associations between criteria pollutants (i.e., fine particulate matter [PM 2.5 ], nitrogen dioxide, and ground-level ozone), 15 PM 2.5 components, and amygdala subregion volumes and relative volume fractions using both single-pollutant linear mixed-effects regression and partial least squares correlation (PLSC) co-exposure modeling approaches. Results No significant associations were detected using single-pollutant models. Rather, in examining mixtures of exposures with PLSC, one latent dimension (52% variance explained) captured a positive association between calcium and several basolateral subregions. Latent dimensions were also identified for amygdala relative volume fractions (ranging from 30% to 82% variance explained), with PM 2.5 and component co-exposure associated with increases in lateral, but decreases in medial and central, relative volume fractions. Conclusions Fine particulate matter and its components are associated with distinct amygdala differences, potentially playing a role in risk for adolescent mental health problems.

关键词： amygdala air pollution PM 2.5 neuroimaging ABCD Study brain development

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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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Single-nucleus transcriptional profiling of the placenta reveals the syncytiotrophoblast stress response to COVID-19

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American Journal of Obstetrics and Gynecology 2025年第4期232卷 S160-S175.e7页

作者： Keuls, Rachel A. Ochsner, Scott A. Miyauchi, Akihiko Campbell, Kadeshia M. Lanners, Natalie Goldstein, Jeffery A. Yee, Connor McKenna, Neil J. Parchem, Ronald J. Parchem, Jacqueline G. Development Disease Models & Therapeutics Graduate Program Baylor College of Medicine Houston TX Department of Molecular and Cellular Biology Baylor College of Medicine Houston TX Center for Cell and Gene Therapy Baylor College of Medicine Houston TX Stem Cells and Regenerative Medicine Center Baylor College of Medicine Houston TX Department of Neuroscience Baylor College of Medicine Houston TX Brotman Baty Institute for Precision Medicine University of Washington Seattle WA United States Department of Obstetrics Gynecology and Reproductive Sciences McGovern Medical School The University of Texas Health Science Center at Houston Houston TX Department of Pathology Northwestern University Feinberg School of Medicine Chicago IL Larry C. Gilstrap MD Center for Perinatal and Women's Health Research The University of Texas Health Science Center at Houston Houston TX

Background: COVID-19 in pregnancy is associated with placental immune activation, inflammation, and vascular malperfusion, but its impact on syncytiotrophoblast biology and function is unclear. Objective: This study aimed to determine the effects of maternal COVID-19 on placental syncytiotrophoblasts using single-nucleus transcriptional profiling and to compare placental stress responses in COVID-19 and preeclampsia. Study Design: For transcriptional characterization of syncytiotrophoblasts, we used the single-nucleus RNA sequencing platform, single-cell combinatorial indexing RNA sequencing (sci-RNA-seq3), to profile placental villi and fetal membranes from unvaccinated patients with symptomatic COVID-19 at birth (n = 4), gestational age-matched controls (n = 4), and a case of critical COVID-19 in the second trimester with delivery at term (n = 1). Clustering of nuclei and differential gene expression analysis was performed in Seurat. Gene ontology analysis was conducted using Enrichr. High-confidence transcriptional target analysis was used to identify key transcription factor nodes governing the syncytiotrophoblast response to maternal SARS-CoV-2 infection. Bioinformatic approaches were further used to compare the COVID-19 dataset to published preeclampsia gene signatures. Tissue analysis, including immunofluorescence, was conducted to validate the transcriptional data and to compare COVID-19 and preeclampsia placental histology for an expanded cohort of placentas: controls (n = 6), asymptomatic COVID-19 (n = 3), symptomatic COVID-19 (n = 5), and preeclampsia with severe features (n = 7). Results: The analyzed dataset comprised 15 cell clusters and 47,889 nuclei. We identified 3 clusters of syncytiotrophoblasts representing fusing and mature nuclei with overlapping but distinct transcriptional responses to COVID-19. Bioinformatic analyses indicated that COVID-19 is associated with the following alterations in syncytiotrophoblasts: (1) endoplasmic reticulum stress

关键词： CEBPB COVID-19 endoplasmic reticulum stress placenta preeclampsia pregnancy SARS-CoV-2 single-nucleus RNA sequencing syncytiotrophoblast transcriptomics trophoblast unfolded protein response

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Sigma-1R-Pom121 axis preserves nuclear transport and integrity in poly-PR-induced C9orf72 ALS

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Neurobiology of disease 2025年 212卷 106992页

作者： Chun-Yu Lin Hsuan-Cheng Wu Ru-Huei Fu Eddie Feng-Ju Weng Wen-Chi Hsieh Tsung-Ping Su Hsiang-En Wu Shao-Ming Wang Neuroscience and Brain Disease Center China Medical University Taichung 404328 Taiwan School of Medicine College of Medicine China Medical University Taichung 404328 Taiwan. Graduate Institute of Biomedical Sciences College of Medicine China Medical University Taichung 404328 Taiwan. Graduate Institute of Biomedical Sciences College of Medicine China Medical University Taichung 404328 Taiwan Ph.D. Program for Aging China Medical University Taichung 404328 Taiwan Translational Medicine Research Center China Medical University Hospital Taichung 40447 Taiwan. Cellular Pathobiology Section Integrative Neuroscience Research Branch Intramural Research Program National Institute on Drug Abuse National Institutes of Health DHHS 333 Cassell Drive Baltimore MD 21224 USA. Graduate Institute of Biomedical Sciences College of Medicine China Medical University Taichung 404328 Taiwan. Electronic address: wangs@mail.cmu.edu.tw.

Nucleocytoplasmic transport disruption contributes to the pathogenesis of C9orf72-associated amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Among the dipeptide repeat proteins translated from G4C2-repeat RNA, poly-PR is particularly toxic, compromising nuclear envelope integrity and transport. Here, we revealed that poly-PR reduced expression of the nucleoporin Pom121 in NSC-34 cells and in an AAV-mediated poly-PR mouse model, resulting in cytoplasmic mislocalization of the neuroprotective transcription factor ATF3 and nuclear envelope damage. Pom121 overexpression restored nuclear ATF3 localization and alleviated poly-PR-induced toxicity. We further identified Sigma-1 receptor (Sigma-1R) as a stabilizer of Pom121 that preserved nuclear integrity and ATF3 function under oxidative stress. Overexpression of Sigma-1R, Pom121, or ATF3 rescued poly-PR-induced cytotoxicity. Our findings defined a protective Sigma-1R/Pom121/ATF3 axis and suggested this pathway as a therapeutic target in C9orf72-linked ALS.

关键词： Atf3 C9orf72 ALS Nuclear envelope integrity Nucleocytoplasmic transport Poly-PR Pom121 Sigma-1R

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Regulation of behavioral responses to single prolonged stress in male and female rats: Role of PACAP

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Neurobiology of Stress 2025年 36卷

作者： Smail, Marissa A. Cotella, Evelin M. Martelle, Susan E. Chambers, James B. Parikh, Ria K. Moore, Christine E. Packard, Ben A. Nawreen, Nawshaba Moloney, Rachel D. Herman, James P. Department of Pharmacology and Systems Physiology University of Cincinnati Cincinnati OH United States Neuroscience Graduate Program University of Cincinnati Cincinnati OH United States Department of Psychology Ohio State University Columbus OH United States Department of Functional and Systems Neuroscience Instituto Mercedes y Martin Ferreyra INIMEC-CONICET Universidad Nacional de Córdoba Córdoba Argentina RAI Services Company Winston-Salem NC United States Program in Neuroscience The University of Maryland School of Medicine Baltimore MD United States Eli Lilli and Company Indianapolis IN United States School of Pharmacy University College Cork Cork Ireland Department of Pharmacology and Therapeutics University College Cork Cork Ireland APC Microbiome Ireland University College Cork Cork Ireland Veterans Affairs Medical Center Cincinnati OH United States Department of Neurology University of Cincinnati Cincinnati OH United States

Post-Traumatic Stress Disorder (PTSD) is a debilitating condition in which a traumatic experience triggers symptoms related to re-experiencing, avoidance, arousal, and mood dysregulation. PTSD negatively impacts 6 % of people during their lifetime, with women being disproportionally affected and exhibiting different, more severe symptoms than men. Despite this widespread impact, the molecular mechanisms underlying PTSD and its sex differences remain poorly understood. Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) is a neuropeptide which participates in fine-tuning circuitry throughout the brain and has been associated with PTSD in humans, especially in women. Here, we use Single Prolonged Stress (SPS), an animal model of PTSD, to explore the roles of PACAP and sex in PTSD-like behaviors. Specifically, a PACAP agonist or antagonist was infused into the infralimbic (IL) prefrontal cortex, a region key to regulating fear- and anxiety-related behaviors, prior to SPS in male and female rats. Rats were then tested in open field/novel object, elevated plus maze, and social interaction. Utilizing a behavioral indexing method, we were able to uncover SPS effects in PTSD-related behavioral domains that were differentially impacted by PACAP manipulations in males and females. While both sexes exhibited increased threat avoidance and decreased threat assessment following SPS, females increased sociability while males decreased sociability. Males also appeared to be protected by IL PACAP antagonism while female SPS phenotypes were exacerbated by IL PACAP agonism. Furthermore, RNAscope revealed that PACAP in the prefrontal cortex responds differently to SPS in males and females. Together, these findings suggest complex relationships between SPS, sex, and IL PACAP which may have important implications for treating PTSD in men and women. © 2025 The Authors

关键词： PACAP Post-traumatic stress disorder Prefrontal cortex Sex Single prolonged stress

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AAA + ATPase Thorase inhibits mTOR signaling through the disassembly of the mTOR complex 1

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Nature Communications 2022年第1期13卷 4836页

作者： Umanah, George K. E. Abalde-Atristain, Leire Khan, Mohammed Repon Mitra, Jaba Dar, Mohamad Aasif Chang, Melissa Tangella, Kavya McNamara, Amy Bennett, Samuel Chen, Rong Aggarwal, Vasudha Cortes, Marisol Worley, Paul F. Ha, Taekjip Dawson, Ted M. Dawson, Valina L. Neuroregeneration and Stem Cell Programs Institute for Cell Engineering Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Neurology Johns Hopkins University School of Medicine Baltimore 21205 MD United States Cellular and Molecular Medicine Graduate Program Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Materials Science and Engineering University of Illinois at Urbana-Champaign Urbana 61801 IL United States Department of Biophysics and Biophysical Chemistry Johns Hopkins University Baltimore 21205 MD United States Solomon H. Snyder Department of Neuroscience Johns Hopkins University School of Medicine Baltimore 21205 MD United States Departments of Biophysics and Biophysical Chemistry Biophysics and Biomedical Engineering JHU Howard Hughes Medical Institute Baltimore 21205 MD United States Department of Pharmacology and Molecular Sciences Johns Hopkins University School of Medicine Baltimore 21205 MD United States Department of Physiology Johns Hopkins University School of Medicine Baltimore 21205 MD United States Division of Neuroscience National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda MD United States Vollum Institute Oregon Health & Science University Portland 97239 OR United States

The mechanistic target of rapamycin (mTOR) signals through the mTOR complex 1 (mTORC1) and the mTOR complex 2 to maintain cellular and organismal homeostasis. Failure to finely tune mTOR activity results in metabolic dysregulation and disease. While there is substantial understanding of the molecular events leading mTORC1 activation at the lysosome, remarkably little is known about what terminates mTORC1 signaling. Here, we show that the AAA + ATPase Thorase directly binds mTOR, thereby orchestrating the disassembly and inactivation of mTORC1. Thorase disrupts the association of mTOR to Raptor at the mitochondria-lysosome interface and this action is sensitive to amino acids. Lack of Thorase causes accumulation of mTOR-Raptor complexes and altered mTORC1 disassembly/re-assembly dynamics upon changes in amino acid availability. The resulting excessive mTORC1 can be counteracted with rapamycin in vitro and in vivo. Collectively, we reveal Thorase as a key component of the mTOR pathway that disassembles and thus inhibits mTORC1. © 2022, The Author(s).

关键词： Cell signalling Lysosomes Mechanisms of disease

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Comparison of endoscopic third ventriculostomy versus cerebrospinal fluid shunt procedures for the treatment of pediatric hydrocephalus in Taiwan

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Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery 2024年第9期40卷 2883-2891页

作者： Shu-Mei Chen Li-Ying Chen Jiann-Her Lin Nicole Salazar Tu-Hsueh Yeh Wei-Lun Lo Tai-Ngar Lui Yi-Chen Hsieh Li-Nien Chien Department of Neurosurgery Taipei Medical University Hospital Taipei Medical University Taipei Taiwan. Department of Surgery School of Medicine Taipei Medical University Taipei Taiwan. Health Data Analytics and Statistics Center Office of Data Science Taipei Medical University Taipei Taiwan. Julius L. Chambers Biomedical/Biotechnology Institute and Department of Biological & Biomedical Sciences North Carolina Central University Durham NC USA. Department of Neurology Taipei Medical University Hospital Taipei Taipei Medical University Taipei Taiwan. Department of Neurology School of Medicine College of Medicine Taipei Medical University Taipei Taiwan. Department of Neurosurgery Shuang Ho Hospital Taipei Medical University Taipei Taiwan. The PhD Program in Medical Neuroscience College of Medical Science and Technology Taipei Medical University 250 Wu-Hsing Street Taipei Taiwan. ychsieh@tmu.edu.tw. Institute of Health and Welfare Policy College of Medicine National Yang Ming Chiao Tung University No.155 Sec. 2 Linong St. Beitou District Taipei Taiwan. linien.chien@nycu.edu.tw. Graduate Institute of Data Science College of Management Taipei Medical University Taipei Taiwan. linien.chien@nycu.edu.tw.

PURPOSE:Pediatric hydrocephalus is the most common cause of surgically treatable neurological disease in children. Controversies exist whether endoscopic third ventriculostomy (ETV) or cerebrospinal fluid (CSF) shunt placement is the most appropriate treatment for pediatric hydrocephalus. This study aimed to compare the risk of re-operation and death between the two procedures. METHODS:We performed a retrospective population-based cohort study and included patients younger than 20-years-old who underwent CSF shunt or ETV for hydrocephalus from the Taiwan National Health Insurance Research Database. RESULTS:A total of 3,555 pediatric patients from 2004 to 2017 were selected, including 2,340 (65.8%) patients that received CSF shunt placement and 1215 (34.2%) patients that underwent ETV. The incidence of all-cause death was 3.31 per 100 person-year for CSF shunt group and 2.52 per 100 person-year for ETV group, with an adjusted hazard ratio (HR) of 0.79 (95% confidence interval [CI] = 0.66-0.94, p = 0.009). The cumulative incidence competing risk for reoperation was 31.2% for the CSF shunt group and 26.4% for the ETV group, with an adjusted subdistribution HR of 0.82 (95% CI = 0.70-0.96, p = 0.015). Subgroup analysis showed that ETV was beneficial for hydrocephalus coexisting with brain or spinal tumor, central nervous system infection, and intracranial hemorrhage. CONCLUSION:Our data indicates ETV is a better operative procedure for pediatric hydrocephalus when advanced surgical techniques and instruments are available.

关键词： Cerebrospinal shunt Pediatric hydrocephalus Reoperation Third ventriculostomy

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Correction to: Effects of low-intensity training on the brain and muscle in the congenital muscular dystrophy 1D model

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Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 2022年第11期43卷 6613页

作者： Clarissa M Comim Jaime A Soares Adriano Alberti Viviane Freiberger Letícia Ventura Paula Dias Aryadnne L Schactae Leoberto R Grigollo Amanda V Steckert Daniel F Martins Rudy J Nodari Junior Mariz Vainzof João Quevedo Research Group in Neurodevelopment of Childhood and Adolescence Laboratory of Experimental Neuroscience Postgraduate Program in Health Sciences University of South Santa Catarina (UNISUL) Avenida Pedra Branca 25 Pedra Branca Palhoça SC 88137‑270 Brazil. Research Group in Neurodevelopment of Childhood and Adolescence Laboratory of Experimental Neuroscience Postgraduate Program in Health Sciences University of South Santa Catarina (UNISUL) Avenida Pedra Branca 25 Pedra Branca Palhoça SC 88137‑270 Brazil. adrianoalberti90@***. Translational Psychiatry Laboratory Graduate Program in Health Sciences University of Southern Santa Catarina (UNESC) Criciúma SC Brazil. Research Department Salus Dermatoglifia Luzerna 89609‑000 Santa Catarina Brazil. Human Genome Research Center Biosciences Institute University of São Paulo São Paulo Brazil. Center of Excellence On Mood Disorders Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth) Houston TX USA. Neuroscience Graduate Program The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Houston TX USA. Translational Psychiatry Program Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth) Houston TX USA.

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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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