Influence of Age on Amyloid Load in Alzheimer's Disease and in Atypical Focal Cortical Alzheimer's Disease (BIOMAGE)
The first objective is to asses influence of age on amyloid load measured by PET imaging using Pittsburgh B compound (PiB) radio-tracer, in Alzheimer's disease(AD). This will allow the determination of brains age-specific deterioration factors by comparing Early onset AD (EOAD), Late onset AD (LOAD)and atypical focal cortical AD (PCA and LPA). The amount of brain lesions in AD patients is estimated by:
- measuring the rate of cortical brain atrophy,
- FDG imaging of glucose metabolism reflecting neuronal activity, and
- for patients who benefited from a lumbar puncture; Cortical-spinal fluid (CSF) amounts of amyloïd and tau proteins are measured.
Posterior Cortical Atrophy
Logopenic Progressive Aphasia
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Influence of Age on amyloïd Load in Alzheimer's Disease and in Atypical Focal Cortical Alzheimer's Disease Like Posterior Cortical Atrophy (PCA) and Logopenic Progressive Aphasia (LPA)Using Positron Emitting Tomography (PET) Imaging|
- PIB-PET imaging of amyloid load [ Time Frame: 0 - 2 months ] [ Designated as safety issue: No ]PET imaging using PIB radio-tracer will give an estimation of regional amyloid load for every patient
- FDG-PET imaging of glucose metabolism [ Time Frame: 0 - 2 months ] [ Designated as safety issue: No ]PET imaging using 18F-fluorodesoxyglucose (FDG) will give a visualization of regional neuronal metabolism
- clinical phenotypic assessment [ Time Frame: 0 - 2 months ] [ Designated as safety issue: No ]the clinical evaluation includes a neurologic consulting, a neuropsychologic assessment of cognitive performances, and evaluation of autonomy
- MRI [ Time Frame: 0 - 2 months ] [ Designated as safety issue: No ]the magnetic resonance imaging will be performed using numerous modalities like T1 weighted sequences for anatomic information, T2 weighted FLAIR and TSE sequences to avoid vascular injuries and T2 GRE to avoid microbleeds, DTI for the diffusion tensor imaging and default mode FMRI, to identify neural networks involved in default concious mode.
- ApoE gene sequencing [ Time Frame: 0 - 24 months after inclusion ] [ Designated as safety issue: No ]ApoE gene sequencing, will be performed after all samples have been collected. So this may be 0 to 24 month after inclusion.
- amyloid and Tau measurements in cerebro-spinal fluid (csf) [ Time Frame: -6 months or +6months arround T0 ] [ Designated as safety issue: No ]some patients have a lumbar puncture that allows a direct quantification of CSF amyloid, tau and phospho-tau amounts.This measure is performed in the 6 months following the clinical assessment (at inclusion) and when a former puncture has already been done, it can be used retro-actively up to 6 months before clinical assessment.
Biospecimen Retention: Samples With DNA
DNA sample immortalized blood cell cultures csf aliquots for patients who beneficiated from a lumbar puncture.
|Study Start Date:||March 2009|
|Study Completion Date:||May 2012|
|Primary Completion Date:||May 2012 (Final data collection date for primary outcome measure)|
EOAD typical AD
this cohort is constituted with early onset typical AD.
this group is constituted with late onset typical AD
this group is constituted with atypical form of focal cortical atrophy, like posterior cortical atrophy and logopenic progressive aphasia.
Literature data suggests there are different types of AD depending on their age of onset, called EOAD and LOAD. These two categories are distinguished by the localization of brain atrophy : severe and 'posterior' in EOAD and more 'anterior' in LOAD. Neuro-pathologic data suggests some atypical focal cortical atrophy, characterized by a respect of episodic memory, may be classified within EOAD.
PiB-based PET imaging allows the in-vivo visualization and quantification of amyloïd load.
We want to answer the question whether the amount of amyloïd protein may be lower in LOAD than EOAD in patients showing the same level of dementia, and thus identify ageing-specific cognitive disorders and understand witch factors influence etio-pathology of typical and atypical Alzheimer's disease.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01095744
|Pitie Salpêtrière Hospital|
|Paris, Ile de France, France, 75651|
|Principal Investigator:||Bruno Dubois, professor doctor||INSERM U975|
|Study Chair:||marie c sarzin, doctor||Inserm U975|