Vanja Nagy, Molecular Neurobiology
email: vanja [dot] nagyrud [dot] lbg [dot] ac [dot] at
The identification of novel genes and elucidation of their regulatory networks are essential in understanding how dysfunctions manifest in neurological pathologies, and to harness those discoveries for the development of efficient therapeutic agents.
Understanding peripheral neuropathies
Congenital insensitivity to pain with anhidrosis (CIPA) is an inherited and rare type of peripheral neuropathy marked by a complete absence of pain perception. By deciphering the pathophysiology of this disease and characterizing the key molecular players, we aim to provide novel targets for future therapy. Although our understanding of the molecular mechanisms underlining nociceptive processing has progressed significantly, effective and non-habit forming therapeutics are still lacking. By detailed analysis of this group of disorders, we aim to identify novel therapeutic targets for pain management relevant for a larger population.
Synaptic plasticity underlying neurodevelopmental disorders
A synapse is a functional unit connecting two neurons, and in relevant regions of the brain is thought to be the epicenter of memory storage. So-called ‘synaptic plasticity’, the ability of the synapse to undergo substantial structural and functional remodeling is indispensable for its function, and is orchestrated by a molecular network of complex intra- and extracellular events. A posttranslational modification, ubiquitination, has recently gained ground as an important event during learning-dependent synaptic activity. A mutation in an E3 ubiquitin ligase has been shown to cause a neurodevelopmental disorder resulting in intellectual disability, spasticity and abnormal gait in young patients. We find that mice lacking this ligase have a remarkably similar phenotype to patients and are an ideal model to study the molecular neuropathology of this disease.
Photo credit - CeMM/WDäuble