Seminars

Matthew J. Girgenti discusses how research on individual brain cells and the three-dimensional organization of DNA is changing the biological understanding of post-traumatic stress disorder. The seminar examines how these approaches reveal trauma-associated brain changes and identify possible targets for more effective, personalized treatments. Girgenti is a neuroscientist in Yale School of Medicine’s Department of Psychiatry. Jeffrey Borenstein moderates this Meet the Scientist session. Online via the BBRF Zoom webinar. Tuesday 13 October 2026, 14:00 EDT (America/New_York; UTC−4). Follow Register Today on the organizer’s event page to the event-specific Zoom form. Advance registration is available to researchers, students, healthcare providers, mental-health organizations, patients and family members.

Brain metabolism supplies the energy underlying brain injury, recovery and aging. This webinar brings together three complementary approaches to understanding how repetitive mild traumatic brain injury affects these processes. Sakthivel Ravi examines repetitive mild TBI and aging through multimodal imaging and molecular profiling. Adam Khalifa presents wireless brain glucose sensing for TBI research, and Joe Abisambra discusses disruption of bioenergetic pathways following repetitive mild TBI. The talks are followed by a moderated question-and-answer discussion.

Astrocytes help sustain neural signaling and tissue stability, but injury and implanted devices cause them to change their functions. Tim O'Shea examines how the extent and timing of this response determine tissue protection, regeneration and implant durability. Limited renewal of adult astrocytes contrasts with the greater proliferation and migration of immature cells in newborn mammals. Around implants, continuing movement, infection and other stimuli can prolong the response and affect device performance. The talk uses astrocyte-specific transcriptomic assays to investigate this reprogramming and considers how to improve repair without sacrificing normal astrocyte functions. It also presents biomaterial and cell-transplant approaches being studied in preclinical stroke, spinal cord injury and implant-response models.

Junjie Guo investigates how an intronic nucleotide-repeat expansion in C9orf72 causes familial and some sporadic cases of amyotrophic lateral sclerosis and frontotemporal dementia. The talk presents progress in understanding how the expansion changes gene expression, alongside functional-genomics approaches that identify potential therapeutic targets controlling expression of the pathogenic mutation. It also considers which mechanisms and modifiers extend to other disease-causing repeat expansions. Guo is Associate Professor of Neuroscience at Yale School of Medicine; the seminar is hosted by J. Wren Kim. Online via CUNY ASRC Zoom. Thursday 8 October 2026, 12:00–13:00 EDT (America/New_York; UTC−4). Follow the Zoom link on the official seminar page; meeting details are also supplied in its abstract PDF. Organized by the Advanced Science Research Center at the CUNY Graduate Center, Neuroscience Initiative. This listing advertises remote attendance.

UCL Department of Neuroinflammation Seminar by Professor Emad Moeendarbary (Professor of Cell Mechanics and Mechanobiology, UCL Mechanical Engineering) on how biophysical factors such as substrate stiffness and axon geometry regulate oligodendrocyte behavior and myelin formation, presenting the AxoMetic in vitro myelination platform for discovery of remyelinating therapies.

Mariana Wolfner presents research on the molecular changes in eggs, sperm, and females that coordinate successful reproduction, drawing on genetic and physiological studies of fertilization. This NIH Wednesday Afternoon Lecture Series event is offered in person and through NIH VideoCast.

Shiv Grewal discusses how chromatin and epigenetic mechanisms establish, maintain, and transmit genome states beyond the DNA sequence itself. This NIH Wednesday Afternoon Lecture Series event is offered in person and through NIH VideoCast.

UC Berkeley Molecular & Cell Biology seminar (Division of Genetics, Genomics & Development) by Barak Cohen of Washington University in Saint Louis on massively parallel experimental studies of enhancer function.

Convergence Seminar by Alexis Battle, PhD (Wu and Zhang Professor of Biomedical Engineering and Computer Science, Johns Hopkins University), on computational and machine-learning approaches for analyzing how genetic variation impacts gene regulation and disease, including noncoding sequences and rare variants.

Jiaqi Zhang examines how computational models can learn the effects of genetic interventions from single-cell experiments. Such experiments reveal causal relationships, but their high-dimensional measurements are costly to collect and difficult to interpret. The seminar connects identifiable causal representations with a predictive method for previously unseen perturbations. The approach incorporates prior biological knowledge and changes in data distributions to estimate responses at individual-cell resolution. It also uses predictions to guide subsequent experiments. An application identifies and experimentally validates previously unknown T-cell regulators with potential relevance to cancer immunotherapy. The recording follows the original July seminar; the series lists Zhang at MIT, while the recording biography describes her incoming Columbia appointment.

Shimon Sakaguchi, Mary E. Brunkow and Fred Ramsdell explain how peripheral immune tolerance prevents the immune system from attacking the body. Sakaguchi follows the identification of regulatory T cells, the CD25 marker, and the relationship between central tolerance and active suppression of self-reactive cells. He considers how changing regulatory T-cell activity could support cancer treatment and transplantation. Brunkow describes genetic investigation of scurfy mice, identification of FOXP3, and the connection between mutations in this gene and human IPEX syndrome. The work establishes a molecular basis for the development and function of regulatory T cells. Ramsdell traces the move from these basic discoveries toward therapeutic strategies, including engineering a patient’s regulatory T cells to target inflammation in rheumatoid arthritis. He discusses early clinical investigation and the ambition of restoring immune balance; these approaches are presented as developing treatments rather than established cures.

Thalamic networks, at the core of thalamocortical and thalamosubcortical communications, underlie processes of perception, attention, memory, emotions, and the sleep-wake cycle, and are disrupted in mental disorders, including schizophrenia and autism. However, the underlying mechanisms of pathology are unknown. I will present novel evidence on key organizational principles, structural, and molecular features of thalamocortical networks, as well as critical thalamic pathway interactions that are likely affected in disorders. This data can facilitate modeling typical and abnormal brain function and can provide the foundation to understand heterogeneous disruption of these networks in sleep disorders, attention deficits, and cognitive and affective impairments in schizophrenia and autism, with important implications for the design of targeted therapeutic interventions

The cortex comprises many neuronal types, which can be distinguished by their transcriptomes: the sets of genes they express. Little is known about the in vivo activity of these cell types, particularly as regards the structure of their spike trains, which might provide clues to cortical circuit function. To address this question, we used Neuropixels electrodes to record layer 5 excitatory populations in mouse V1, then transcriptomically identified the recorded cell types. To do so, we performed a subsequent recording of the same cells using 2-photon (2p) calcium imaging, identifying neurons between the two recording modalities by fingerprinting their responses to a “zebra noise” stimulus and estimating the path of the electrode through the 2p stack with a probabilistic method. We then cut brain slices and performed in situ transcriptomics to localize ~300 genes using coppaFISH3d, a new open source method, and aligned the transcriptomic data to the 2p stack. Analysis of the data is ongoing, and suggests substantial differences in spike time coordination between ET and IT neurons, as well as between transcriptomic subtypes of both these excitatory types.

Cellular crosstalk is an essential process during brain development and is influenced by numerous factors, including cell morphology, adhesion, the local extracellular matrix and secreted vesicles. Inspired by mutations associated with neurodevelopmental disorders, we focus on understanding the role of extracellular mechanisms essential for the proper development of the human brain. Therefore, we combine 2D and 3D in vitro human models to better understand the molecular and cellular mechanisms involved in progenitor proliferation and fate, migration and maturation of excitatory and inhibitory neurons during human brain development and tackle the causes of neurodevelopmental disorders.

David Reich examines how sequencing DNA from ancient human remains has changed the reconstruction of population history. Genetic evidence from past cultures can reveal relationships and movements that are difficult to infer from living populations alone, sometimes challenging interpretations based on archaeology, language and written history. The lecture explores what these discoveries imply for understanding shared and complex human ancestries, and how knowledge of the past could inform the study of human health. A discussion with Carl Zimmer connects the research to the interpretation and communication of evidence about human history. The programme extends the paleogenomic research associated with the 2022 medicine prize through recent work on ancient and modern human DNA.

Nervous system function relies on the polarized architecture of neurons, established by directional transport of pre- and postsynaptic cargoes. While delivery of postsynaptic components depends on the secretory pathway, the identity of the membrane compartment(s) that supply presynaptic active zone (AZ) and synaptic vesicle (SV) proteins is largely unknown. I will discuss our recent advances in our understanding of how key components of the presynaptic machinery for neurotransmitter release are transported and assembled focussing on our studies in genome-engineered human induced pluripotent stem cell-derived neurons. Specifically, I will focus on the composition and cell biological identity of the axonal transport vesicles that shuttle key components of neurotransmission to nascent synapses and on machinery for axonal transport and its control by signaling lipids. Our studies identify a crucial mechanism mediating the delivery of SV and active zone proteins to developing synapses and reveal connections to neurological disorders. In the second part of my talk, I will discuss how exocytosis and endocytosis are coupled to maintain presynaptic membrane homeostasis. I will present unpublished data regarding the role of membrane tension in the coupling of exocytosis and endocytosis at synapses. We have identified an endocytic BAR domain protein that is capable of sensing alterations in membrane tension caused by the exocytotic fusion of SVs to initiate compensatory endocytosis to restore plasma membrane area. Interference with this mechanism results in defects in the coupling of presynaptic exocytosis and SV recycling at human synapses.