Research Questions
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.
04 Feb 2010
Responses: 2
Neuroinflammation is proposed to be a major factor in creating a toxic environment in the PD brain. However, what is the contribution of the adaptive immune system (ie. T cell function) to PD pathogenesis, and how can we target this system for future therapeutic approaches?
03 Feb 2010
Responses: 1
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.
25 Jan 2010
Responses: 9
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?
08 Jan 2010
Responses: 5
What are the next practical steps for identifying Parkinson’s disease subtypes that can be useful in guiding treatment and therapeutic development?
This question arose from discussion at a recent MJFF Executive Scientific Advisory Board meeting of the outcomes from the Foundation's '2007 PD Subtypes Program'. Read more details here. Members can post all comments and questions by hitting the 'create response' button on this research question. MJFF will summarize and announce the conclusions of this effort after sufficient discussion has taken place.
23 Dec 2009
Responses: 8
PD Online member Dr. Andrew Singleton (NIH/NIA) poses the following questions to start this discussion about the future of PD genetics:
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What will be the
impact of the $1000 genome on PD genetics and what are the roadblocks to
success? - Can we presently understand gene and environment interactions? Will new technologies reveal the interface between genetics and the environment?
- Is there a role for somatic mutation in Parkinson's disease?
- What are the ethical considerations as we approach a more complete understanding of the genetic and epigenetic architecture of PD?
- What would you do with a billion dollars earmarked for genetic research?
23 Dec 2009
Responses: 5
