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Completed

NCT Number: NCT01095744

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

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.

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Key information

Conditions

Alzheimer's Disease Alzheimer Disease Amyloidosis Brain Diseases Central Nervous System Diseases Cognition Disorders Cognitive Dysfunction Dementia Logopenic Progressive Aphasia Mental Disorders Metabolic Diseases Nervous System Diseases Neurocognitive Disorders Neurodegenerative Diseases Nutritional and Metabolic Diseases Posterior Cortical Atrophy Proteostasis Deficiencies Tauopathies

Age range

18 year and older

Sex eligibility

All sexes

Study type

Observational

Primary location

Pitie Salpêtrière Hospital

Paris, Île-de-France Region, 75651, France

About this study

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.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

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

Treatment and study plan

Primary outcomes

  1. PIB-PET imaging of amyloid load

    Time frame: 0 - 2 months

    PET imaging using PIB radio-tracer will give an estimation of regional amyloid load for every patient

  2. FDG-PET imaging of glucose metabolism

    Time frame: 0 - 2 months

    PET imaging using 18F-fluorodesoxyglucose (FDG) will give a visualization of regional neuronal metabolism

  3. clinical phenotypic assessment

    Time frame: 0 - 2 months

    the clinical evaluation includes a neurologic consulting, a neuropsychologic assessment of cognitive performances, and evaluation of autonomy

  4. MRI

    Time frame: 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.

  5. ApoE gene sequencing

    Time frame: 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 outcomes

  1. amyloid and Tau measurements in cerebro-spinal fluid (csf)

    Time frame: -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.

Sponsors and collaborators

Lead sponsor

Institut National de la Santé Et de la Recherche Médicale, France

Other Gov

Registry information

Official study 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

Acronym: BIOMAGE

Important dates

Study start
2009
Primary completion
2012
Study completion
2012
First posted
Mar 30, 2010
Registry last updated
Oct 7, 2025

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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