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

NCT ID: NCT01095744

Last Updated: 2025-10-07

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

60 participants

Study Classification

OBSERVATIONAL

Study Start Date

2009-03-31

Study Completion Date

2012-05-31

Brief Summary

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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

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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.

Conditions

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Alzheimer's Disease Posterior Cortical Atrophy Logopenic Progressive Aphasia

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Study Groups

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EOAD typical AD

this cohort is constituted with early onset typical AD.

No interventions assigned to this group

LOAD typical

this group is constituted with late onset typical AD

No interventions assigned to this group

atypical AD

this group is constituted with atypical form of focal cortical atrophy, like posterior cortical atrophy and logopenic progressive aphasia.

No interventions assigned to this group

young controls

under 65

No interventions assigned to this group

old controls

over 65

No interventions assigned to this group

Eligibility Criteria

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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
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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

OTHER_GOV

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Bruno Dubois, professor doctor

Role: PRINCIPAL_INVESTIGATOR

INSERM U975

marie c sarzin, doctor

Role: STUDY_CHAIR

Inserm U975

Locations

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Pitie Salpêtrière Hospital

Paris, Île-de-France Region, France

Site Status

Countries

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France

References

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Dorothee G, Bottlaender M, Moukari E, de Souza LC, Maroy R, Corlier F, Colliot O, Chupin M, Lamari F, Lehericy S, Dubois B, Sarazin M, Aucouturier P. Distinct patterns of antiamyloid-beta antibodies in typical and atypical Alzheimer disease. Arch Neurol. 2012 Sep;69(9):1181-5. doi: 10.1001/archneurol.2012.604.

Reference Type RESULT
PMID: 22710357 (View on PubMed)

Migliaccio R, Agosta F, Toba MN, Samri D, Corlier F, de Souza LC, Chupin M, Sharman M, Gorno-Tempini ML, Dubois B, Filippi M, Bartolomeo P. Brain networks in posterior cortical atrophy: a single case tractography study and literature review. Cortex. 2012 Nov-Dec;48(10):1298-309. doi: 10.1016/j.cortex.2011.10.002. Epub 2011 Oct 20.

Reference Type RESULT
PMID: 22099855 (View on PubMed)

de Souza LC, Corlier F, Habert MO, Uspenskaya O, Maroy R, Lamari F, Chupin M, Lehericy S, Colliot O, Hahn-Barma V, Samri D, Dubois B, Bottlaender M, Sarazin M. Similar amyloid-beta burden in posterior cortical atrophy and Alzheimer's disease. Brain. 2011 Jul;134(Pt 7):2036-43. doi: 10.1093/brain/awr130.

Reference Type RESULT
PMID: 21705422 (View on PubMed)

Other Identifiers

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2008-A00939-46

Identifier Type: REGISTRY

Identifier Source: secondary_id

C08-30

Identifier Type: -

Identifier Source: org_study_id

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