Influence of Age on Amyloid Load in Alzheimer's Disease and in Atypical Focal Cortical Alzheimer's Disease

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

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT01095744

Acronym

BIOMAGE

Enrollment

Registered

2010-03-30

Start date

2009-03-31

Completion date

2012-05-31

Last updated

2025-10-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Alzheimer's Disease, Logopenic Progressive Aphasia, Posterior Cortical Atrophy

Keywords

PIB imaging,, brain atrophy, cognitive impairment, Pet imaging, Alzheimer's disease, amyloid protein

Brief summary

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: 1. measuring the rate of cortical brain atrophy, 2. FDG imaging of glucose metabolism reflecting neuronal activity, and 3. for patients who benefited from a lumbar puncture; Cortical-spinal fluid (CSF) amounts of amyloïd and tau proteins are measured.

Detailed description

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.

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Yes

Inclusion criteria

* AD patients: clinical dementia rating between 0.5 and 2 free and cued recall test (Grober and Buschke) cued-recall \< 18/48 and total recall \< 40/48 * atypical AD : i visual-spatial disorder and respect of episodic memory progressive evolution, Balint syndrome ii progressive language disorder constituted of logopenic aphasia respect of episodic memory * controls: age over 30 MMSE over or equal to 27 normal neuropsychiatric state for age and education level

Exclusion criteria

* for every patients : psychiatric disorders age under18 absence of social security counter indication to MRI supposed or actual alcoholism or drug addiction pregnancy

Design outcomes

Primary

Measure	Time frame	Description
FDG-PET imaging of glucose metabolism	0 - 2 months	PET imaging using 18F-fluorodesoxyglucose (FDG) will give a visualization of regional neuronal metabolism
clinical phenotypic assessment	0 - 2 months	the clinical evaluation includes a neurologic consulting, a neuropsychologic assessment of cognitive performances, and evaluation of autonomy
PIB-PET imaging of amyloid load	0 - 2 months	PET imaging using PIB radio-tracer will give an estimation of regional amyloid load for every patient
MRI	0 - 2 months	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	0 - 24 months after inclusion	ApoE gene sequencing, will be performed after all samples have been collected. So this may be 0 to 24 month after inclusion.

Secondary

Measure	Time frame	Description
amyloid and Tau measurements in cerebro-spinal fluid (csf)	-6 months or +6months arround T0	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.

Countries

France

Outcome results