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.

Tom Nowakowski explains lineage barcoding and single-cell sequencing approaches for reconstructing neural stem-cell family trees and early wiring programs in developing mouse and human brains.

Lindsay N. Oberman reviews evidence for transcranial magnetic stimulation protocols in autism spectrum disorder. The seminar first explains how TMS works and how it can probe the brain mechanisms associated with autism. It then presents NIH research using repetitive TMS as an experimental therapeutic tool, examining its effects on both brain function and behaviour to guide the development of potential interventions. Online via Duke Zoom. Wednesday 7 October 2026, 16:00 EDT (America/New_York; UTC−4). Register through the event-specific Register Here link on the Duke Autism Seminar Series page to receive remote access. The presentation will not be recorded. Accommodation requests should reach the organizer at least ten days before the event. The speaker directs NIMH’s Developmental Clinical Neurophysiology and Neurostimulation Research Program.

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.

Vanessa Siffredi explores why the corpus callosum is central to typical brain development, yet some children born without it or with callosal abnormalities develop comparably to their peers. The talk connects callosal structure and communication between hemispheres with cognition, attention, executive function, memory, language and socio-emotional development. Structural and functional neuroimaging studies of typical development and callosal dysgenesis examine how developing brains compensate for alterations in this major white-matter pathway. Siffredi is affiliated with CHUV and UNIL; Carole Guedj chairs the seminar. Hybrid: Auditoire de pédiatrie Fred Bamatter, HUG, Hôpital des Enfants, Geneva; online via Zoom. Tuesday 29 September 2026, 09:30–10:30 CEST (Europe/Zurich; UTC+2), followed by CIBM news and networking until 11:00. Organized by CIBM Center for Biomedical Imaging — Breakfast and Science. In-person attendance is free without registration. Remote attendees must register through the Zoom link on the event page and select the 29 September occurrence.

Bryce Mander presents research on early sleep biomarkers associated with Alzheimer's disease pathophysiology and memory impairment. The William C. Dement Seminar connects sleep and circadian neuroscience with neurodegeneration, cognition and clinically relevant approaches to detecting disease-related change.

Yuko Munakata presents evidence challenging capacity-only accounts of self-control and explains how experience, effort, and expected payoff shape executive-function engagement and later outcomes.

Nick Turk-Browne presents research using infant functional MRI to investigate how the hippocampus supports learning and memory early in life. The seminar connects neural development, memory formation and infantile amnesia through new methods for studying awake infants.

The Nature versus Nurture debate has generally been considered from the lens of genome versus experience dichotomy and has dominated our thinking about behavioral individuality and personality traits. In contrast, the role of nonheritable noise during brain development in behavioral variation is understudied. Using the Drosophila melanogaster visual system, I will discuss our efforts to dissect how individuality in circuit wiring emerges during development, and how that helps generate individual behavioral variation.

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.

Neuroplasticity is essential for the establishment and strengthening of neural circuits. Repetitive transcranial magnetic stimulation (rTMS) is commonly used to modulate cortical excitability and shows promise in the treatment of some neurological disorders. Low intensity magnetic stimulation (LI-rTMS), which does not directly elicit action potentials in the stimulated neurons, have also shown some therapeutic effects, and it is important to determine the biological mechanisms underlying the effects of these low intensity magnetic fields, such as would occur in the regions surrounding the central high-intensity focus of rTMS. Our team has used a focal low-intensity (10mT) magnetic stimulation approach to address some of these questions and to identify cellular mechanisms. I will present several studies from our laboratory, addressing (1) effects of LIrTMS on neuronal activity and excitability ; and (2) neuronal morphology and post-lesion repair. The ensemble of our results indicate that the effects of LI-rTMS depend upon the stimulation pattern, the age of the animal, and the presence of cellular magnetoreceptors.