Prof. Dr. Frank Bradke—Senior Group Leader at the DZNE and Professor at the University of Bonn—has been welcomed as a new member of the North Rhine–Westphalia Academy of Sciences and Arts. He received his certificate from the Academy’s President, Prof. Dr. Gerd Heusch, in a ceremony held earlier this year. Bradke’s research focuses on the molecular and cellular mechanisms behind axonal growth and regeneration in the central nervous system—work that underpins his standing as a leading international neurobiologist . He studied biochemistry, anatomy, and developmental biology in Berlin and London, completed his PhD at EMBL Heidelberg, and conducted postdoctoral research at UCSF and Stanford. Prior to his current roles, he led a research group at the Max Planck Institute in Martinsried. He has been a member of the Leopoldina since 2014 and was awarded the prestigious Gottfried Wilhelm Leibniz Prize in 2016. —For more details, see the University of Bonn announcement:https://www.uni-bonn.de/de/neues/frank-bradke-in-die-nrw-akademie-der-wissenschaften-und-der-kuenste-aufgenommen

Prof. Dr. Frank Bradke, neurobiologist at the German Center for Neurodegenerative Diseases (DZNE) and professor at the University of Bonn, has been elected to the Berlin-Brandenburg Academy of Sciences and Humanities (BBAW). The induction ceremony took place on June 14, 2025, in Berlin. Bradke is internationally recognized for his research on axonal growth and nerve regeneration in the central nervous system, particularly following spinal cord injuries. His work combines cellular models with animal studies to uncover mechanisms that promote or inhibit neuronal repair. Among many honors, he received the Leibniz Prize (2016), the Roger de Spoelberch Prize (2018), and the BBAW Academy Award (2024). He is a member of several leading scientific organizations, including the Leopoldina and the Academia Europaea. More information:

We warmly congratulate our group leader Dr. Tobias Ackels on receiving the prestigious Paul Ehrlich and Ludwig Darmstaedter Early Career Award 2025. The Paul Ehrlich Foundation honors his groundbreaking research on how the olfactory system contributes to memory processes and emotional behavior. This award is one of the most important distinctions for early career scientists in Germany and highlights the outstanding quality and impact of his scientific work. Further information can be found in the official announcements byUniversity of Bonn,UKB Newsroom,Research in Germany, andGoethe University Frankfurt.

Wie entsteht Erinnerung? Unser Kollege Florian Mormann geht dieser spannenden Frage auf den Grund – mit Konzeptneuronen im menschlichen Gehirn! In DIE ZEIT am Wochenende (Ausgabe 22/2025) gibt’s einen großen Artikel über seine Forschung. Online nachzulesen (leider hinter der Bezahlschranke):https://lnkd.in/eWiCApnk

Tobias Ackels awarded for pioneering research on scent perception and brain function Dr. Ackels’ pioneering work has revealed that mammals can process olfactory information at an astonishing speed—up to 40 times per second, far exceeding their breathing rate. This challenges the long-standing belief that the sense of smell is slow and highlights the critical role of temporal dynamics in sensory perception. His findings not only advance our understanding of how the brain interprets sensory signals but also suggest potential applications in early dementia detection, as olfactory impairments are often among the first signs of neurodegenerative diseases. Dr. Ackels, who recently joined the University of Bonn from the Francis Crick Institute in London, leads the „Sensory Dynamics and Behaviour“ research group at the Institute for Experimental Epileptology and Cognitive Science at UKB. His work, supported by an ERC Starting Grant, combines animal behaviour and advanced imaging and electrophysiological techniques with computational modelling to study neuronal activity in real time. The award ceremony will take place on March 14, 2025, at 5 p.m. in Frankfurt’s Paulskirche, alongside the main Paul Ehrlich Prize 2025. For more details, visit:https://www.uni-bonn.de/de/neues/015-2025 https://www.ukbnewsroom.de/tobias-ackels-erhaelt-paul-ehrlich-und-ludwig-darmstaedter-nachwuchspreis/ https://www.research-in-germany.org/idw-news/en_US/2025/1/2025-01-28_A_gateway_to_memory__Paul_Ehrlich_and_Ludwig_Darmstaedter_Early_Career_Award_2025_goes_to_Tobias_Ackels.html https://aktuelles.uni-frankfurt.de/english/a-gateway-to-memory-paul-ehrlich-and-ludwig-darmstaedter-early-career-award-2025-goes-to-tobias-ackels/ For inquiries: Prof. Dr. Tobias Ackels – tobias.ackels@ukbonn.de Congratulations to Prof. Dr. Tobias Ackels on this outstanding recognition! Written by: Michela Barboni, Ph.D

Researchers at the University of Bonn have revealed how genetic predisposition and environmental factors, such as neuroinflammation, interact to influence neuronal development and contribute to autism spectrum disorders. Bonn, November 28 – Researchers at the University of Bonn have uncovered new insights into how genetic predisposition and environmental factors converge to shape neuronal development, potentially contributing to autism spectrum disorders (ASD). This work highlights the intricate interplay between genetic risk factors and neuroinflammation in the developing brain and offers a mechanistic explanation for how these elements combine to influence neurodevelopment. Autism is a complex neurological developmental disorder that impacts social interaction, communication, and perception. While both genetic and environmental contributors are recognized, the precise mechanisms underlying their interaction have remained unclear. The research team, led by Stephan Baader at the Anatomical Institute, focused on Purkinje cells—key neurons in the cerebellum known for their critical role in cerebellar function and structural organization—to investigate these interactions. The study utilized cerebellar slice cultures to probe the combined effects of genetic overexpression of the autism susceptibility gene Engrailed-2 and inflammatory stimulation using lipopolysaccharide (LPS), an agent known to mimic bacterial infection. Results demonstrated that LPS reduced dendritic growth in Purkinje cells, an effect exacerbated by the overexpression of Engrailed-2. This reduction in dendritic growth could be mitigated by inhibiting microglial proliferation or blocking tumor necrosis factor-alpha (TNF-α) receptor signaling, highlighting the pivotal role of microglia and TNF-α in this process. The implications of these findings are profound. They suggest that while genetic and environmental risk factors alone may have limited penetrance in causing ASD symptoms, their combination significantly increases the risk. This highlights the importance of considering both genetic susceptibility and environmental exposures, such as prenatal infections, in understanding ASD pathogenesis. The study, titled „Genetic and environmental risk factors cooperate to affect autistic-like neuronal...

New insights from the Epi25 Collaborative highlight the complex genetic architecture of epilepsy, identifying distinct ultra-rare genetic risk factors across various disorder subtypes through the largest whole-exome sequencing study conducted to date. Bonn, October 2024 – Identifying genetic risk factors for the highly heterogeneous disorder of epilepsy has long been a challenge for researchers. In a pivotal study, the Epi25 Collaborative has conducted what is believed to be the largest whole-exome sequencing analysis of epilepsy to date, involving over 54,000 human exomes. This extensive research includes 20,979 deeply phenotyped patients from diverse genetic ancestry groups and 33,444 controls, shedding light on the rare variants that contribute to disease risk. Our Bonn group has contributed 2,546 patient samples to this study which included samples from 59 study centers. Epilepsy, characterized by recurrent seizures, encompasses a variety of subtypes, making the understanding of its genetic underpinnings complex. The findings of this study implicate seven individual genes, three gene sets, and four copy number variants that reach exome-wide significance. Notably, genes associated with ion channels demonstrate strong links to multiple epilepsy subtypes, including epileptic encephalopathies, generalized epilepsies, and focal epilepsies. In contrast, many of the other gene discoveries appear to be subtype-specific, underscoring the distinct genetic contributions associated with different forms of epilepsy. The researchers combined data from rare single-nucleotide variants, short insertion and deletion variants, copy number variants, and common variants to present an expanded view of epilepsy’s genetic architecture. Their analyses revealed increasing evidence of convergence among various genetic risk loci affecting the same genes. The top candidate genes identified are notably enriched for roles in synaptic transmission and neuronal excitability, particularly during postnatal development and in the neocortex. Interestingly, this study also highlights shared rare variant risks between epilepsy and other neurodevelopmental disorders, suggesting overlapping genetic vulnerabilities. To facilitate further...

Bonn researchers uncover how seizure-related focal spreading depolarization contributes to abnormal post-ictal behaviors in epilepsy. Bonn, October 12 – Understanding the neurobiological mechanisms underlying post-ictal symptoms in epilepsy such as confusion, aphasia, and unaware wandering, which are most frequently observed in temporal lobe epilepsy (TLE), has long been a challenge for researchers. A pivotal study led by Prof. Wenzel and his team at Bonn University has revealed the critical role of seizure-associated focal spreading depolarization (sSD) as a pathoclinical factor in epilepsy, providing new insights into post-ictal states. In this comprehensive investigation, the researchers employed advanced imaging techniques, including two-photon and widefield imaging, alongside field potential and single-unit recordings, to study seizures in both murine models and human subjects. The study began with observations of seizures during viral encephalitis in mice and subsequently developed an optogenetic strategy to differentiate between hippocampal seizures and spreading depolarization. The findings demonstrated that sSD occurs in a region-specific manner, displaying distinct spatial trajectories in relation to preceding seizures. Notably, both seizure-related sSD and isolated hippocampal SD were found to trigger post-ictal wandering behavior, even without the progression of sSD to the neocortex. This unexpected locomotor phenotype highlights a previously unrecognized pathway through which seizures can affect behavior following the ictal state. Moreover, the researchers confirmed the existence of sSD in human epilepsy patients using Behnke-Fried electrode recordings. The patterns observed in humans were consistent with those identified in murine models, indicating a common neurobiological mechanism. The implications of these findings are significant for both epilepsy research and clinical practice. Notably, due to the current international EEG standard, sSD is invisible in clinical practice. Thus, by uncovering sSD as a crucial factor underlying post-ictal behavioral abnormalities, this study challenges existing standards in EEG monitoring and raises important questions about the traditional understanding of post-ictal states...