Division of Pain Volume Transmission

Our research

Headache disorders are some of the most common neurological disorders, and they carry a huge socioeconomic cost. Furthermore, a majority of patients suffering from headache does not have sufficient effect of currently available therapies.

In our group, the aim is to delineate the non-synaptic signaling pathways that drive headache in migraine and other headache disorders as well as in neurological diseases where headache is a part of the symptomatology. In a mouse model of migraine with aura, we recently showed that increased glymphatic washout of cortical proteins associated with inflammatory processes drove substantial changes in the cerebrospinal fluid proteome. We identified a flow route where cerebrospinal fluid permeates the large trigeminal ganglion that carries peripheral sensory information from the head. The transport of proteins released during migraine aura towards the trigeminal ganglion drove increased activity in sensory neurons that transmit pain information. Thus, we have identified several new proteins that might be driving the initial activation of the sensory system in migraine with aura.
 
Currently, we are exploring the role of these proteins in the development of the migraine phenotype and we are investigating downstream signaling matrices between the brain, peripheral sensory system, and other cell clusters activated in headache disorders. Our goal is to identify pathways that can be used to develop new medicine that can prevent and abort headache. To this end, we use an array of neuroscience tools including transgenic animal models, optogenetics, in vivo imaging, mass spectrometry proteomics, transcriptomics, magnetic resonance imaging, behaviour and histology.