Both conditions show a similar loss of dopaminergic neurons and associated cognitive and motor function deficits, but their disease progression differ profoundly in terms of time and brain pathology—Prof Barker believes they should be dealt with differently. Image: Victor GonzalezAN exceptional collaborative research study is being undertaken by neuroscientists at Edith Cowan University in WA and the Cambridge Centre for Brain Repair (CCBR) in the UK.
To explain why patients with Parkinson’s disease (PD) display different clinical deficits and vary in disease progression over time, patients are followed from diagnosis onwards.
Professor Roger Barker, Cambridge-based neurologist and Deputy Director of the CCBR, and Dr Meghan Thomas, Research Fellow at ECU and Founding Director of its Parkinson’s Centre ‘ParkC’, share the belief that recognition of essentially different clinical features and genetic profiles in PD enhances the potential for targeted treatment.
“Our aim is to determine if PD is composed of clinically distinct subtypes, each with their own pathology and disease history”, says Dr Thomas.
Both collaborators run their own prospective patient cohort studies at different side of the globe to verify the overlap of specific PD-subgroups in different populations and to validate new therapies for them.
Prof Barker’s initiative to use longitudinal studies in PD-research provides unprecedented insight into the natural history of the disease.
“If you could follow the cohort for 30 years, most of them would have developed dementia at the end of the day”, he says.
However, 20–30 percent already suffer from dementia in early PD.
These patients follow the most malignant course of disease progression, whereas the PD-course of the remainder of patients could be labelled as more benign.
Both conditions show a similar loss of dopaminergic neurons and associated cognitive and motor function deficits, but their disease progression differ profoundly in terms of time and brain pathology—Prof Barker believes they should be dealt with differently.
“The development of dementia is not just a consequence of a decline in cognition”, says Prof Barker.
To slow down further neurodegeneration, PD-patients with dementia are best off with disease modifying therapies, like exercise and anti-inflammatory drugs. All others may benefit more from therapies geared towards delaying the onset of dementia like cell transplantation.
His dual pathway concept in PD is supported by distinct difference in genes involved in either dopamine turnover or more general cell metabolism to survive.
Parallel studies by both neuroscientists focus on neurogenesis and the therapeutic application of foetal tissue and stem cells for transplantation to improve outcomes in early PD-patients.
Prof Barker recently visited Perth to present this research programme to various audiences, including the local PD-community at the annual ‘ParkC’ Open Day.
