My colleagues Katharina Heil, Emilia Wysocka, Oksana Sorokina, Jeanette Hellgren, Ian Simpson, Douglas Armstrong and I have published a manuscript on bioRxiv that describes our work to determine how many of the the proteins found in synapses have been included in computational, biophysical models of synapses. The answer is not very many: We were able to map only 4.2% of previously reported synaptic proteins to entities in biophysical models.

We cross-linked the set of modelled proteins with sets of genes associated with common neurological diseases. We find some examples ofo disease-associated molecules that are well represented in models, such as voltage-dependent calcium channel family (CACNA1C), dopamine D1 receptor, and glutamate ionotropic NMDA type 2A and 2B receptors. Many other disease-associated genes have not been included in models of synaptic plasticity, for example catechol-O-methyltransferase (COMT) and MAOA. By incorporating pathway enrichment results, we identify LAMTOR, a gene uniquely associated with Schizophrenia, which is closely linked to the MAPK pathway found in some models.