Research Questions
What do recent epidemiological and laboratory results with caffeine tell us about developing A2A based therapies?
Find here a short-list of PD papers added to Pubmed in the last week. Has one caught your eye? Is your favorite paper not on the list? Should one of these not have made the cut? Add your comments below by logging in and posting a response.
The development of rodent models of LID has improved our ability to conduct studies into the molecular mechanisms of LID as well as to screen new therapeutic strategies. However, it is much harder to detect and analyze rodent behavior relevant to L-DOPA-induced abnormal movements than in primate models. Which behavioral outcomes are relevant in rodent models of dyskinesia?
Is PD-associated fatigue truly a distinctly different symptom from PD-associated sleep disturbance? If so, is this thought to be due to separate anatomic substrates or biological factors involved with each? Conversely, if they stem from a common cause, does one necessarily go hand-in-hand with the other?
What are the best strategies for developing effective therapies for fatigue and sleep-related problems in PD?
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?
Parkin and PINK1 are two genes implicated in autosomal recessive Parkinson's disease. Parkin is an E3 ligase and a component of the ubiquitin-proteasome system involved in protein turnover while the function of PINK1 is still unclear. Biochemical studies have linked the two in a molecular pathway that entail mitochondrial function, yet how parkin and PINK1 interact, and how these two proteins affect mitochondrial function remains a mystery.
