PD map meets the Community

The PD map had its first trip abroad – destination Switzerland. With the van filled to the brim with the PD map touch screen, workshop material and a bunch of scientists, we set out for Geneva to run our first curation workshop at the “XX World Congress on Parkinson’s Disease and Related Disorders”. 

 

Why a curation workshop? 

Already during the content development for the early version of the PD map it was quite obvious that a comprehensive repository of PD pathways needs expertise in many domains of molecular neuropathology, and beyond. One small team cannot simply know it all. We needed a group of experts to tell us what is expected, content- and functionality-wise, from a resource like the PD map. More than a year ago, when Henning Hermjakob visited LCSB, an idea was born to organize a curation workshop of PD-related pathways for this purpose. 

The “XX World Congress on Parkinson’s Disease and Related Disorders” in Geneva seemed the ideal place to meet with PD experts from various areas, With the great support of the organizing committee we had arranged our workshop as satellite event of the conference. The goal was the curation of “hallmark” pathways (advert here) – mitochondrial dysfunction, protein misfolding or neuroinflammation. In the morning of December 8th 2013 about 40 people, including clinicians, senior researcher, post-docs and PhD students, joined us in Hall C of Palexpo, Geneva. Broad range of topics has been discussed, as briefly summarized below.

 

α-synuclein pathobiology

We have talked about functional interactions of synuclein with special emphasis to different species having distinct function, especially in the context of the spreading hypothesis. We were also suggested to include the effects of nitrosylations on synuclein and to incorporate the work of Gendelman and co-workers describing its relations to adaptive immunity in PD. Finally, reports on synuclein phosphorylation (PLK2 and PLK3) were marked as important.

Mitochondrial dysfunction

Although the PD map already features certain mechanisms around PGC1-alpha, more details are needed. We particularly discussed the incorporation of PGC1-alpha involvement in the regulation of mitochondrial biogenesis and its links to PD pathology. Another suggestion for improvement was to curate in detail the impact of mitochondrial DNA damage on neurodegeneration.

Neuroinflammation

 “There is no PD without inflammation,” we have heard during the discussion on neuroinflammatory pathways and PD. Still, the role of inflammation in PD - cause or consequence, triggers, or exacerbation – remains unexplored. Metabolism of reactive oxygen species, glutathione (GSTP1 in particular) and dopamine were suggested as critical extensions of the map. Another challenging suggestion was to incorporate blood-brain barrier related mechanisms to represent interactions of substantia nigra cells with components of systemic inflammatory processes.

Functionality

We have received a number of constructive suggestions on how to improve the interface of the map. The most frequent requests were: functionality to represent drug targets and drug metabolism; visualization of biomarkers and clinical endpoints; and, last but not least, a straightforward way to visualize custom experimental data on the map. 

 

The meeting with the members of scientific community was extremely useful – it showed us the most important directions we are expected to go. The voice of clinical researchers, a numerous group among the participants, was our reality check. Careful curation of a number of PD pathways is not sufficient to support translation of the knowledge on molecular pathology of PD to the clinics. With that though in mind, we sit down to do our homework. 

  

Marek Ostaszewski

Curator/Developer

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