Parkinson's disease is characterized by a large number of non motor, especially neuropsychiatric, signs. Their pathophysiology is complex but the role of dopaminergic and serotoninergic systems dysfunction is suggested by several studies. In addition, the serotoninergic system is involved in the pathophysiology of dyskinesias. Very few studies have analyzed the abnormalities of these two neurotransmission systems at disease onset, in de novo PD patients. Furthermore, the parallel evolution of the degeneration of the dopaminergic and serotoninergic systems with disease progression remains unknown. Thus the present study aims at determining, by using PET and 11C-PE2I and 11C-DASB the respective role of the serotoninergic and dopaminergic systems dysfunction in motor and non motor manifestations in PD, at different evolution stages.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
49
Hospices Civils de Lyon, Hopital Neurologique Pierre Wertheimer
Bron, France
Respective progression of both dopaminergic and serotoninergic lesions in Parkinson's disease
Dopaminergic lesions will be determined by positron emission tomography (PET) using 11C-PE2I in 3 groups of PD patients (de novo; mid-stage (4-7 years of evolution); late-stage (8-10 years of evolution). Serotoninergic lesions will be assessed by positron emission tomography (PET) using 11C-DASB in the same 3 groups of PD patients. In addition a control group will be included.
Time frame: This will be achieved at the end of the inclusion period, thus 24 to 36 months after study onset (January 2014).
Correlations between neuropsychiatric observed in Parkinson's disease at different stages of evolution
Dopaminergic lesions will be determined by positron emission tomography (PET) using 11C-PE2I in 3 groups of PD patients (de novo; mid-stage (4-7 years of evolution); late-stage (8-10 years of evolution). Serotoninergic lesions will be assessed by positron emission tomography (PET) using 11C-DASB in the same 3 groups of PD patients. In addition a control group will be included. The neuropsychiatric manifestations studied are : * hypo and hyperdopaminergic signs : ECMP scale * Apathy using LARS scale * Anxiety using BAI scale * Depression using BDI scale (Beck Depression Inventory) * Affective well-being and asthenia using visual analogic scales of Norris * MATHYS scale * Global cognitive scale : MATTIS * Food behavior using TFEQ scale * Personality : TCI-R scale * Impulsivity by UPPS scale
Time frame: These correlations will be determined at the end of the inclusion period, thus 24 to 36 months after study onset (January 2014).
Role of dopaminergic and serotoninergic lesions in fatigue
: Dopaminergic lesions will be determined by positron emission tomography (PET) using 11C-PE2I in 3 groups of PD patients (de novo; mid-stage (4-7 years of evolution); late-stage (8-10 years of evolution). Serotoninergic lesions will be assessed by positron emission tomography (PET) using 11C-DASB in the same 3 groups of PD patients. In addition a control group will be included. Fatigue will be assessed using the PDFS-16 scale
Time frame: This will be determined at the end of the inclusion period, thus 24 to 36 months after study onset (January 2014).
Relationship between the severity of dopaminergic and serotoninergic lesions and the quality of life
Dopaminergic lesions will be determined by positron emission tomography (PET) using 11C-PE2I in 3 groups of PD patients (de novo; mid-stage (4-7 years of evolution); late-stage (8-10 years of evolution). Serotoninergic lesions will be assessed by positron emission tomography (PET) using 11C-DASB in the same 3 groups of PD patients. In addition a control group will be included. Fatigue will be assessed using the PDQ39 (Parkinson's Disease Questionnaire) scale
Time frame: These correlations will be determined at the end of the inclusion period, thus 24 to 36 months after study onset (January 2014).
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