Molecular and Functional Imaging in SNCA, Parkin and PINK1
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT04084509|
Recruitment Status : Not yet recruiting
First Posted : September 10, 2019
Last Update Posted : September 10, 2019
Parkinson's Disease (PD) is a progressive neurodegenerative disease characterized clinically by bradykinesia, resting tremor, rigidity, and postural instability. The hallmark pathophysiological alteration is a loss of dopaminergic transmission across the nigrostriatal pathway. According to Braak's neuropathological staging of disease, the pathological process in PD occurs in a gradual ascending fashion, starting from the olfactory bulb and progressing to the brainstem, with preferential involvement of the raphe nuclei, which contain serotonergic nuclei, and the noradrenergic locus coeruleus, before involving the substantia nigra and thereafter the whole brain. Little is known about the mechanisms underlying neuronal degeneration in PD and currently, no treatment is available to halt disease progression in PD. The pathophysiological characterisation of phenomena occurring in the time window between the pathological start of the disease and the onset of motor symptoms is crucial to develop potential neuroprotective agents. Several genes causing, the so-called monogenic parkinsonism, have been discovered providing important insights on the pathogenesis of PD.
The objective of the study is to characterize the molecular phenomena underlying genetic forms of parkinsonism and, therefore, providing further insights about the possible mechanisms taking place in PD and help identify targets for disease-modifying therapeutics, by using PET imaging with [11C]DASB (a marker of Serotonin transporter), SPECT imaging using [123I]FP-CIT (a marker of the presynaptic Dopamine transporter), and multi-modal MRI imaging, clinical markers (motor and non-motor symptoms and neuropsychological battery), blood and CSF biomarkers.
|Condition or disease|
|Parkinson Disease PARK1 PARK2|
|Study Type :||Observational|
|Estimated Enrollment :||44 participants|
|Official Title:||Molecular and Functional Imaging of Parkinson's Pathology in SNCA, Parkin and PINK1 Mutation Carriers|
|Estimated Study Start Date :||October 1, 2019|
|Estimated Primary Completion Date :||September 30, 2022|
|Estimated Study Completion Date :||September 30, 2022|
|Idiopathic Parkinson's Disease|
|Symptomatic Genetic Carriers (SNCA, Parkin or PINK1)|
|Asymptomatic Genetic Carriers (SNCA, Parkin or PINK1)|
- Primary Outcomes [ Time Frame: Up to 21 days ]To quantify serotonergic and dopaminergic pathology in carriers of genetic mutations for familial forms of Parkinsonism, idiopathic PD patients and healthy controls.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04084509
|Contact: Marios Politis, MD MSc PhDemail@example.com|
|Contact: Chloe Farrell, PhDfirstname.lastname@example.org|
|Principal Investigator:||Marios Politis, MD MSc PhD||King's College London|