Research Questions
Evidence suggests that exercise can have symptomatic benefits in patients with PD, though it is unclear whether these effects are equally beneficial to the parkinsonian brain. Given the numerous different forms of exercise available, it is worth exploring whether one form is more valuable than another for PD patients.
02 Jul 2009
Responses: 3
Current theory suggests a possible toxic oligomeric or aggregated form of alpha-synuclein as the trigger for subsequent neurodegeneration in PD, but definitive evidence for this is lacking. Proposed therapeutic approaches focus predominately on breaking up aggregates, or attempt to reduce alpha-synuclein protein levels, either by inhibiting production (e.g, via RNA interference) or enhancing protein turnover. Given current understanding of alpha-synuclein, are these the best approaches for targeting alpha-synuclein therapeutically? What studies are needed to clarify the ideal alpha-synuclein target?
03 Jul 2009
Responses: 3
There is evidence of oxidative damage in brains of PD patients and anti-oxidant therapies have been explored as disease-modifying therapies for PD. Alpha-synuclein aggregation - in the form of Lewy bodies - is the pathological hallmark of PD. If it a link could be determined between these two pathogenic processes, targeting this common pathway may be a viable approach for developing novel disease-modifying therapies.
01 Jul 2009
Responses: 1
PD therapeutics development presents many trial design challenges, such as, for example, the difficulty of measuring changes in disease progression, and the inherent variability in clinical assessments of dyskinesia that result from ongoing dyskinesia-inducing drug treatment. How can novel clinical trial designs, and modifications of traditional trial designs, meet these challenges? What are the strengths and weaknesses of these design approaches?
01 Jul 2009
Responses: 1
There is some evidence that different forms of Parkinson's disease exist and that the severity of disease course may be linked to these possible subtypes. To date, there is little understanding of what differentiates these patient populations from one another, either clinically or pathologically. Is there evidence for a genetic link? What are the clinical differences?
01 Jul 2009
Responses: 5
Mutations in the gene coding for the putative kinase LRRK2 represent
some of the most prevalent genetic factors yet linked to Parkinson’s
disease, but how these alterations lead to PD-related pathogenesis
remains unclear. A prevailing hypothesis centers around the belief that mutations lead to a toxic gain-of-function in kinase activity; thus, identification of substrates of LRRK2 kinase activity is essential to determining the pathogenic mechanism of LRRK2.
28 Jun 2009
Responses: 1
