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Biology subjects

Lendemeijer, B.

Publications and source records attributed to Lendemeijer, B..

7 recordsLinked to original sources

In vitro reconstitution of hippocampal cell assemblies

Three-dimensional neuronal cultures, such as brain organoids, have proven effective for in vitro modeling of brain development and disease. However, it remains unclear whether these systems can intrinsically generate the spatiotemporal network motifs that support cognitive function, particularly given their lack of sensory input. To address this, we developed a 3D long-range modular neuronal network approach to test whether dissociated embryonic hippocampal cells can self-organize into neuronal manifolds capable of generating network dynamics analogous to the in vivo hippocampal cell assemblies implicated in cognitive function. Using all-optical interrogation, we demonstrate in vitro recapitulation of cell assemblies and their hallmark features, including recurring sequential activation, hierarchical chaining, multi-day stability, resilience to perturbation, and attractor-like pattern completion. We further investigated the effects of acute ketamine exposure on these assemblies, revealing network-wide reconfiguration reminiscent of in vivo responses. Finally, we show that human iPSC-derived neurons can similarly self-organize into modular network architectures. Together, these findings are consistent with an intrinsically "inside-out" view of the brain, rather than a tabula rasa model in which sensory input is required for the emergence of cognitive network motifs, and open new avenues for in vitro modeling of network-level mechanisms relevant to neuropsychiatric disorders.

neuroscience↗

Influenza A Virus Infection Impairs Neuronal Activity in Human iPSC-Derived NGN2 Neural Co-Cultures

Influenza A virus (IAV) infection is associated with a wide variety of neurological complications, of which mild complications like impaired cognitive functioning are most prominent. Even though several studies have shown that many influenza viruses can enter the CNS, the neuropathogenesis of seasonal (H3N2 and H1N1) and pandemic (pH1N1 2009) IAV infections is poorly understood. Therefore, we aimed to investigate the cellular tropism, replication efficiency and associated functional consequences using a human stem cell-derived neural co-culture model of neurons and astrocytes. All viruses were able to infect neurons in the co-culture model, although this infection did not result in efficient replication and release of progeny virus. In addition, infection did not result in visible cell death or apoptosis. However, functional analyses revealed that IAV inoculation resulted in a reduction of spontaneous neural activity and a partial reduction of neural excitability. This study shows that seasonal and pandemic IAVs can disrupt neural homeostasis, without efficient virus replication or the induction of cell death. However, these functional changes in neural activity can contribute to cognitive problems during IAV infections in the acute and potentially post-acute phase of the infection.

microbiology↗

Genomic and Transcriptomic Signatures of SETD1A Disruption in Human Excitatory Neuron Development and Psychiatric Disease Risk

Genetic disruption of SETD1A markedly increases the risk for schizophrenia. To elucidate the underlying mechanisms, we generated isogenic organoid models of the developing human cerebral cortex harboring a SETD1A loss-of-function schizophrenia risk mutation. Employing chromatin profiling combined with RNA sequencing, we identified high-confidence SETD1A target genes, analyzed the impact of the mutation on SETD1A binding and transcriptional regulation and validated key findings with orthogonal approaches. Disruption of SETD1A function disturbs the finely tuned temporal gene expression in the excitatory neuron lineage, yielding an aberrant transcriptional program that compromises key regulatory and metabolic pathways essential for neurodevelopmental transitions. Although overall SETD1A binding remains unchanged in mutant neurons, we identified localized alterations in SETD1A binding that correlate with shifts in H3K4me3 levels and gene expression. These changes are enriched at enhancer regions, suggesting that enhancer-regulated genes are especially vulnerable to SETD1A reduction. Notably, target genes with enhancer-bound SETD1A are primarily linked to neuronal functions while those with promoter-bound SETD1A are enriched for basic cellular functions. By mapping the SETD1A binding landscape in excitatory neurons of the human fetal frontal cortex and integrating multimodal neuroimaging and genetic datasets, we demonstrate that the genomic context of SETD1A binding differentially correlates with macroscale brain organization and establish a link between SETD1A-bound enhancers, schizophrenia-associated brain alterations and genetic susceptibility. Our study advances our understanding of the role of SETD1A binding patterns in schizophrenia pathogenesis, offering insights that may guide future therapeutic strategies.

neuroscience↗

iPSC-derived healthy human astrocytes selectively load miRNAs targeting neuronal genes into extracellular vesicles

Astrocytes are in constant communication with neurons during the establishment and maturation of functional networks in the developing brain. Astrocytes release extracellular vesicles (EVs) containing microRNA (miRNA) cargo that regulates transcript stability in recipient cells. Astrocyte released factors are thought to be involved in neurodevelopmental disorders. Healthy astrocytes partially rescue Rett Syndrome (RTT) neuron function. EVs isolated from stem cell progeny also correct aspects of RTT. EVs cross the blood-brain barrier (BBB) and their cargo is found in peripheral blood which may allow non-invasive detection of EV cargo as biomarkers produced by healthy astrocytes. Here we characterize miRNA cargo and sequence motifs in healthy human astrocyte derived EVs (ADEVs). First, human induced Pluripotent Stem Cells (iPSC) were differentiated into Neural Progenitor Cells (NPCs) and subsequently into astrocytes using a rapid differentiation protocol. iPSC derived astrocytes expressed specific markers, displayed intracellular calcium transients and secreted EVs. miRNAs were identified by RNA-Seq on astrocytes and ADEVs and target gene pathway analysis detected brain related terms. The miRNA profile was consistent with astrocyte identity, and included approximately 80 miRNAs found in astrocytes that were relatively depleted in ADEVs suggestive of passive loading. About 120 miRNAs were relatively enriched in ADEVs and motif analysis discovered binding sites for RNA binding proteins FUS, SRSF7 and CELF5. miRNA-483-5p was the most significantly enriched in ADEVs. This miRNA regulates MECP2 expression in neurons and has been found differentially expressed in blood samples from RTT patients. Our results identify potential miRNA biomarkers selectively sorted into ADEVs and implicate RNA binding protein sequence dependent mechanisms for miRNA cargo loading.

molecular biology↗

Rapid specification of human pluripotent stem cells to functional astrocytes

Astrocytes are essential for the formation and maintenance of neural networks through metabolic support, facilitation of synaptic function, and optimization of electrophysiological activity. However, a major technical challenge for investigating astrocyte function and disease-related pathophysiology has been the limited ability to obtain functional human astrocytes. Here we present a novel method to efficiently differentiate human pluripotent stem cell (hPSC)-derived neural progenitors to functional astrocytes in 28 days using a culture medium containing leukemia inhibitory factor (LIF) and bone morphogenetic protein 4 (BMP4). This approach yields highly pure populations of astrocytes expressing canonical astrocyte markers, which we confirmed by immunofluorescence, flow cytometry and RNA sequencing. Human PSC-derived astrocytes efficiently buffer glutamate and robustly support neural network activity. Co-cultures of hPSC-derived astrocytes and neurons on multi-electrode arrays generated robust network activity within 2 days and synchronous network bursts after 6 days. Whole cell patch-clamp recordings revealed an increased frequency of postsynaptic currents in human hPSC-derived neurons co-cultured with hPSC-derived versus primary rodent astrocytes, consistent with a corresponding increase in synapse density. Furthermore, hPSC-derived astrocytes retained their hominid morphology when transplanted into a mouse brain. In conclusion, we present a novel protocol to obtain functional astrocytes from human pluripotent stem cells, providing a platform for investigating human astrocyte function and neuronal-glial interactions.

neuroscience↗

Replication kinetic, cell tropism and associated immune responses in SARS-CoV-2 and H5N1 virus infected human iPSC derived neural models

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is associated with a wide variety of neurological complications. Even though SARS-CoV-2 is rarely detected in the central nervous system (CNS) or cerebrospinal fluid, evidence is accumulating that SARS-CoV-2 might enter the CNS via the olfactory nerve. However, what happens after SARS-CoV-2 enters the CNS is poorly understood. Therefore, we investigated the replication kinetics, cell tropism, and associated immune responses of SARS-CoV-2 infection in different types of neural cultures derived from human induced pluripotent stem cells (hiPSCs). SARS-CoV-2 was compared to the neurotropic and highly pathogenic H5N1 influenza A virus. SARS-CoV-2 infected a minority of individual mature neurons, without subsequent virus replication and spread, despite ACE2, TMPRSS2 and NPR1 expression in all cultures. However, this sparse infection did result in the production of type-III-interferons and IL-8. In contrast, H5N1 virus replicated and spread very efficiently in all cell types in all cultures. Taken together, our findings support the hypothesis that neurological complications might result from local immune responses triggered by virus invasion, rather than abundant SARS-CoV-2 replication in the CNS.

microbiology↗

Novel genetic loci affecting facial shape variation in humans

The human face represents a combined set of highly heritable phenotypes, but knowledge on its genetic architecture remains limited despite the relevance for various fields of science and application. A series of genome-wide association studies on 78 facial shape phenotypes quantified from 3-dimensional facial images of 10,115 Europeans identified 24 genetic loci reaching genome-wide significant association, among which 17 were previously unreported. A multi-ethnic study in additional 7,917 individuals confirmed 13 loci including 8 unreported ones. A global map of polygenic face scores assembled facial features in major continental groups consistent with anthropological knowledge. Analyses of epigenomic datasets from cranial neural crest cells revealed abundant cis-regulatory activities at the face-associated genetic loci. Luciferase reporter assays in neural crest progenitor cells highlighted enhancer activities of several face-associated DNA variants. These results substantially advance our understanding of the genetic basis underlying human facial variation and provide candidates for future in-vivo functional studies.

genomics↗