To me, research is a joy and a passion, not just “a job.” I began my research career in 1999 because I wanted to learn more about how the brain works. To me, the brain is the most fascinating organ in the body, and I wanted to understand how we think, learn and feel. Later, I became more interested in how these mechanisms are disturbed in brain disorders.
It struck me that most brain disorders do not have good treatment options yet. Therefore, while I am still very interested in the basic brain mechanisms, I am now more dedicated to bridging the gap between brain disorders and treatments.
The overarching purpose of my research is to identify and understand pathological molecular mechanisms which contribute to autism and epilepsy. My lab works to discover how these mechanisms affect neuronal and brain function. Our ultimate goal is using this knowledge to identify molecular biomarkers and develop therapeutic strategies.
In more recent years, parts of my lab have tried to identify potential novel brain treatments. We discovered that a PI3K isoform-selective inhibitor ameliorates disease-relevant phenotypes in mouse models for two different neurodevelopmental brain disorders. We also discovered that a specific microRNA regulates neuronal hyperexcitability in mouse models of epilepsy.
My work has been funded by the National Institutes of Health (NIH) and other organizations, such as the Brain and Behavior Research Foundation, the American Epilepsy Society, and the Fragile X Syndrome Research and Treatment (FRAXA) Research Foundation.
Diploma in Biochemistry: Ruhr University Bochum, Germany, 2000.
PhD: Free University of Berlin, Germany, 2004.
Molecular neuroscience, fragile X syndrome
Estradiol- and Progesterone-Associated Changes in microRNA-Induced Silencing and Reduced Antiseizure Efficacy of an Antagomir in Female Mice. eNeuro. 2023; 10:eneuro.0047-eneu22.2023.
Editorial: Forebrain control of breathing and sudden death in epilepsy. Frontiers in Neural Circuits. 2023; 17:1212172.
Neurovascular Development in Pten and Tsc2 Mouse Mutants. eNeuro. 2023; 10:ENEURO.0340-ENEU22.2023.
Some (Syn)Gaps are Worse than Others: Deciphering The Role of Syngap Isoforms in Excitatory Synaptic Function. Epilepsy Currents. 2022; 22:312-314.
A sound-driven cortical phase-locking change in the Fmr1 KO mouse requires Fmr1 deletion in a subpopulation of brainstem neurons. Neurobiology of Disease. 2022; 170:105767.
Impact of Raptor and Rictor Deletion on Hippocampal Pathology Following Status Epilepticus. Journal of Molecular Neuroscience. 2022; 72:1243-1258.
Epilepsy Research Now in 3D: Harnessing the Power of Brain Organoids in Epilepsy. Epilepsy Currents. 2022; 22:135-136.
PARVing the Way to Cap Translation for Seizure Control. Epilepsy Currents. 2021; 21:360-362.
GABAA Alpha 2,3 Modulation Improves Select Phenotypes in a Mouse Model of Fragile X Syndrome. Frontiers in Psychiatry. 2021; 12:678090.