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Spatial architecture of autism pathogenesis reveals mosaic structural disarray during early development.
Autism spectrum disorder (ASD) has been associated with diverse genetic factors and molecular changes. Yet, how pathophysiology emerges during development and contributes to clinical heterogeneity remains unclear. Here we use spatial and single-cell transcriptomics of genetically diverse patient-derived organoids of the prenatal cortex to map the spatial architecture of ASD pathogenesis. We find abnormal partitioning of progenitor and neuron zones alongside local patches of disorganized neurons that vary in distribution among patients. Such spatially mosaic disarray persists into neuronal maturation and is consistent with impaired adhesion between progenitors. Our findings suggest that the spatial landscape of biological processes leading to ASD may be more heterogeneous than previously thought. We propose a model in which different patterns of scattered abnormalities, arising from spatially mosaic pathogenesis during prenatal brain development, contribute to the wide range of symptoms and brain structure variations observed in ASD patients.
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Macro-bio-ethical Versus Micro-bio-ethical Issues Concerning Human Brain Organoids.
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[Ultrastructural aspects of acute cerebral ischemia after treatment with barbiturates].
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Slow and rapid transport of protein to nerve endings in mouse brain.
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Microglial involvement in autism spectrum disorder: insights from human data and iPSC models.
Autism spectrum disorder (ASD) presents a range of lifelong challenges in social communication, repetitive behaviors, and restricted interests, affecting over 2% of the preschool population. Early neurodevelopmental disruptions, particularly those affecting microglia, appear to be central to the pathophysiology of ASD, with microglia influencing synaptic development and stability in the brain. However, the neurobiological mechanisms underlying ASD are still not fully understood. Traditional ASD studies, which rely on animal models and postmortem tissues, have limitations in capturing human-specific neurodevelopmental dynamics. Recent advances in human model systems, including induced pluripotent stem cell (iPSC)-derived neural cultures and brain organoids, offer promising insights into microglia-neuron interactions relevant to ASD. This review evaluates current research using human-based models to explore ASD pathophysiology, focusing on the role of microglia in neurodevelopment, and discusses the strengths and future potential of these innovative approaches.
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PM2.5 induces developmental neurotoxicity in cortical organoids.
There is mounting evidence implicating the potential neurotoxic effects of PM2.5 during brain development, as it has been observed to traverse both the placental barrier and the fetal blood-brain barrier. However, the current utilization of 2D cell culture and animal models falls short in providing an accurate representation of human brain development. Consequently, the precise mechanisms underlying PM2.5-induced developmental neurotoxicity in humans remain obscure. To address this research gap, we constructed three-dimensional (3D) cortical organoids that faithfully recapitulate the initial stages of human cerebral cortex development. Our goal is to investigate the mechanisms of PM2.5-induced neurotoxicity using 3D brain organoids that express cortical layer proteins. Our findings demonstrate that exposure to PM2.5 concentrations of 5 μg/mL and 50 μg/mL induces neuronal apoptosis and disrupts normal neural differentiation, thereby suggesting a detrimental impact on neurodevelopment. Furthermore, transcriptomic analysis revealed PM2.5 exposure induced aberrations in mitochondrial complex I functionality, which is reminiscent of Parkinson's syndrome, potentially mediated by misguided axon guidance and compromised synaptic maintenance. This study is a pioneering assessment of the neurotoxicity of PM2.5 pollution on human brain tissues based on 3D cortical organoids, and the results are of great significance in guiding the formulation of the next air pollution prevention and control policies in China to achieve the sustainable improvement of air quality and to formulate pollution abatement strategies that can maximize the benefits to public health.
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Scanning and transmission electron microscopy on bulk prepared neuronal and glial cells.
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Ultrastructure of the neurosecretory system of the Colorado potato beetle, Leptinotarsa decemlineata (Say). I. Characterization of the protocerebral neurosecretory cells.
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iPSC-Derived 3D Brain Organoids as Next-generation Platforms to Study Viral and Toxicant-associated Neurodegeneration.
Neurodegenerative diseases (ND) are one of the most fatal diseases that affect the majority of individuals worldwide, among which Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common. In vitro 2D monolayer cell cultures and in vivo transgenic animal models have been the primary tools for investigating mechanisms of neurodegenerative diseases. However, the ineffectiveness of these models in translating outcomes into human pathophysiology, necessitates innovative approaches to bridge the translational gap. In this review, we focus on the intricate pathogenic processes by which environmental toxicants and viral infections trigger neurodegeneration. The growing significance of three-dimensional (3D) brain organoids (BOs) derived from induced pluripotent stem cells (iPSCs) can be used as a groundbreaking platform for examining neurodegenerative pathways induced by exposure to environmental toxicants and viral infections. It also addressed how BO's overcomes the fundamental limitations of traditional models, such as 2D cultures and animal models, thereby creating novel opportunities for the mechanistic study of multifactorial neurodegeneration and the development of therapeutic interventions.
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Enzymic activities associated with membranous cytoplasmic bodies and isolated brain lysosomes.