Modeling the progression of Parkinson's Disease: comparison of subjects with and without Sleep Disorders

International audiencePatients with idiopathic Parkinson’s Disease (iPD) may have very different patterns ofprogression, corresponding to distinct disease subtypes. Here, we describe quantitatively theoverall pattern of progression in subgroups of PD by using a Bayesian non-linear mixed effectmodel that describes the continuous progression of biomarkers at both population andindividual level. This approach allows to model variability in progression patterns and diseasestage between patients. We analyzed two subgroups of patients, with (iPD-RBD+) and withoutsleep disorders (iPD-RBD-), that are known to present different patterns of progression [1]. Wecompared the two groups by extracting the ordering of abnormalities that occurred over thedisease course, and by studying their disease onset and speed of progression

Follow-up study of the GIGYF2 gene in French families with Parkinson's disease

Meeus et al. (2009) reported no pathogenic mutations in a comprehensive genetic analysis of the entire GRB10-interacting GYF protein-2 gene (GIGYF2) in a Belgian series of both familial and sporadic patients with Parkinson's disease (PD). Although we initially proposed that GIGYF2 corresponds to the PARK11 locus, in familial PD, we found no causative variations in a follow-up study in which GIGYF2 was screened in an independent series of 185 patients with autosomal dominant PD, mostly of French origin. Together, these results do not support a major role of GIGYF2 in PD

Amantadine use in the French prospective NS-Park cohort

International audienceObjective: To assess amantadine use and associated factors in the patients with Parkinson's disease (PD).Background: Immediate-release amantadine is approved for the treatment of PD and is largely used in clinical practice to treat "levodopa-induced dyskinesia (LIDs). Its use varies according to countries and PD stages. The prospective NS-Park cohort collects features of PD patients followed by 26 French PD Expert Centres.Methods: Variables used for the analyses included demographics, motor and non-motor PD symptoms and motor complications [motor fluctuations (MFs), LIDs)], antiparkinsonian pharmacological classes and levodopa equivalent daily dose (LEDD). We evaluated: (i) prevalence of amantadine use and compared clinical features of amantadine users vs. non-users (cross-sectional analysis); (ii) factors associated with amantadine initiation (longitudinal analysis); (iii) amantadine effect on LIDs, MFs, apathy, impulse control disorders and freezing of gait (Fog) (longitudinal analysis).Results: Amantadine use prevalence was 12.6% (1,585/12,542, median dose = 200 mg). Amantadine users were significantly younger, with longer and more severe PD symptoms, greater LEDD and more frequent use of device-aided/surgical treatment. Factors independently associated with amantadine initiation were younger age, longer PD duration, more frequent LIDs, MFs and FoG, higher LEDD and better cognitive function. 9 of the 658 patients on amantadine had stopped it at the following visit, after 12-18 months (1.3%). New users of amantadine presented a higher improvement in LIDs and MF compared to amantadine never users.Conclusions: About 12% of PD patients within the French NS-Park cohort used amantadine, mostly those with younger age and more severe PD. Amantadine initiation was associated with a subsequent reduction in LIDs and MFs