Following on from the success of previous WPCs in Washington and Glasgow, the third such congress took place in the autumnal sun of early October in Montréal and sought once more to bring patients, carers, medical practitioners, scientists and therapists together under one roof to discuss one condition – Parkinson’s disease (PD).

The ambition of the congress is to enable the dialogue and better understanding of the diseases by linking those with the condition and those seeking to help treat it at whatever level. As such the programme is an interesting mix – ranging from detailed science to live performances of patient inspired artistic endeavours. Each day began with hot topics picked from the numerous posters and was followed by plenary sessions that tackled a host of topics but which in summary covered:

  • The prion like behaviour of alpha synuclein and how this may modify our thinking about disease pathogenesis and spread, as well as therapeutically;
  • The genes linked to PD and how they may need to be expressed through environmental risk factors and the role, if any,  of inflammation in this process;
  • The extent and significance of non-motor symptoms in patients at diagnosis and through the disease course;
  • The cognitive deficits seen in PD, their basis and imaging correlates and how this relates to the development of the dementia of PD;
  • The new therapies being tried in PD including cell, gene and environmental / exercise based approaches;
  • The importance of the patient in driving their own care and research and how this can best be achieved in the context of multidisciplinary teams.

This was followed by a special lecture including the inaugural James Parkinson lecture delivered by Warren Olanow, who eloquently took us through the history of discovery in PD including the original videos of Hornykiewizcz showing the effects of dopa in a patient with PD in the early 1960s – an experiment that could now not be done without a huge amount of paperwork and approval! Thereafter there were a collection of parallel sessions and workshops that covered a plethora of topics including protein misfolding, mitophagy and new gene / cell based approaches.

So in summary the major take home messages were:

  • That PD may begin as a disorder outside of the CNS that is triggered by a misfolding of alpha synuclein which then spreads and causes pathology along neural networks through a prion like behaviour with an early synaptic pathology;
  • The cellular pathology of PD involves a dynamic interplay between proteins, leading to altered mitochondrial and lysosomal function, which may create a positive feedback on alpha synuclein aggregation accelerating the disease process in some cells;
  • The non motor features of PD, especially many of the cognitive abnormalities, significantly impact on quality of life and need to be better recognised, their basis defined and their treatment improved;
  • The ability to treat PD through environmental and physical therapies needs to be aggressively pursued as it holds much promise and may be a very effective intervention at all stages of disease and should not be trumped by more “sexy” therapies involving genes, cells and small molecules.