Research Questions
What do recent epidemiological and laboratory results with caffeine tell us about developing A2A based therapies?
15 Mar 2010
Responses: 0
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.
15 Mar 2010
Responses: 14
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?
15 Mar 2010
Responses: 1
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?
12 Mar 2010
Responses: 0
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?
12 Mar 2010
Responses: 2
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.
04 Mar 2010
Responses: 8
An important step in moving novel neuroprotective agents towards the clinic involves testing the efficacy of therapeutics in preclinical models. Many different preclinical models are available for PD research and decisions about their specific use depends on the particular therapeutic/mechanism under investigation. However, some general issues arise when designing these preclinical tests and controversy exists as to the best outcome measures that should be employed.
24 Feb 2010
Responses: 15
As is the case in other diseases, the current gold standard methodology
for testing the efficacy of experimental Parkinson’s disease
therapeutics involves the placebo-controlled study design. However,
positive placebo responses have been reported in a number of PD trials,
complicating the interpretation of efficacy results. These findings
make interpretation of potential efficacy of an experimental treatment
in an open-labeled study design extremely difficult and also raise the
barriers for the design and interpretation of placebo-controlled trials
in PD. Furthermore, as is the case with other diseases, the underlying
basis for the placebo response in PD patients is poorly understood.
19 Feb 2010
Responses: 10
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. Furthermore, whether (and how) LRRK2 might relate to other PD-related factors has yet to be determined. The observation of varied alpha-synuclein and tau-related pathology in some post-mortem tissue from people with LRRK2-linked PD suggests a complex mechanistic picture.
12 Feb 2010
Responses: 4
Mitochondrial
dysfunction has been found in brain and other body tissue in
Parkinson's disease patients. Additionally, many environmental agents
implicated in PD, such as pesticides, function as mitochondrial
inhibitors. The exact role for mitochondrial function in the etiology
of PD remains controversial.
11 Feb 2010
Responses: 7