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The NINDS supports a broad range of studies aimed at discovering the cause(s) of Parkinson's disease, finding better treatments,
and ultimately preventing and curing the disorder. In 2000 a working group established the Parkinson's Disease Research Agenda
initiating a planning process to ensure that extraordinary opportunities to move toward a cure are adequately supported and
that critical obstacles to progress are addressed. In 2002 a Summit was convened to gain a better sense of where the field
of PD research stands internationally, and to collect information on the "roadblocks" that may still be impacting progress.
This led to the development of the Parkinson's Matrix which identifies additional goals that can help facilitate PD research.
This NIH disease specific website was developed to facilitate research efforts on Parkinson's Disease, track the progress
of the PD Research agenda and Matrix activities, and provides both the research and lay community with information and resources.
The Parkinson's disease research portfolio is managed by the NINDS Neurodegeneration Group.
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We previously reported a linkage region on chromosome 1p (LOD p 3.41) for genes controlling age at onset in Parkinson disease (PD). This region overlaps with the previously reported PARK10 locus. To identify the gene(s) associated with AAO and risk of PD in this region, we first applied a genomic convergence approach that combined gene expression and linkage data. No significant results were found. Second, we performed association mapping across a 19.2-Mb region centered under the AAO linkage peak. An iterative association mapping approach was done by initially genotyping single-nucleotide polymorphisms at an average distance of 100 kb apart and then by increasing the density of markers as needed. Using the overall data set of 267 multiplex families, we identified six associated genes in the region, but further screening of a subset of 83 families linked to the chromosome 1 locus identified only two genes significantly associated with AAO in PD: the g subunit of the translation initiation factor EIF2B gene (EIF2B3), which was more significant in the linked subset and the ubiquitin-specific protease 24 gene (USP24). Unexpectedly, the human immunodeficiency virus enhancer-binding protein 3 gene (HIVEP3) was found to be associated with risk for susceptibility to PD. We used several criteria to define significant results in the presence of multiple testing, including criteria derived from a novel cluster approach. The known or putative functions of these genes fit well with the current suspected pathogenic mechanisms of PD and thus show great potential as candidates for the PARK10 locus.
Mood disorders are the most common psychiatric problem associated with Parkinson's disease (PD), and have a negative impact on disability and quality of life. Accurate diagnosis of depressive disturbances in PD is critical and will facilitate the testing and use of new interventions; however, there are no clear diagnostic criteria for depressive disorders in PD. In their current form, strict Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria are difficult to use in PD and require attribution of specific symptoms to PD itself or the depressive syndrome. Additionally, DSM criteria for major depression and dysthymia exclude perhaps half of PD patients with comorbid clinically significant depression. This review summarizes an NIH-sponsored workshop and describes recommended changes to DSM diagnostic criteria for depression for use in PD. Participants also recommended: (1) an inclusive approach to symptom assessment to enhance reliability of ratings in PD and avoid the need to attribute symptoms to a particular cause; (2) the inclusion of subsyndromal depression in clinical research studies of depression of PD; (3) the specification of timing of assessments for PD patients with motor fluctuations; and (4) the use of informants for cognitively impaired patients. The proposed diagnostic criteria are provisional and intended to be defined further and validated but provide a common starting point for clinical research in PD-associated depression. (c) 2005 Movement Disorder Society.
Last updated August 13, 2008