Implications of Amyloid Pathology
Recruitment status was Recruiting
The purpose of this study is to determine whether asymptomatic older individuals with high amyloid burden will subsequently manifest cognitive impairment and eventually progress to clinical Alzheimer's Disease (AD).
|Study Design:||Observational Model: Cohort
Time Perspective: Cross-Sectional
|Official Title:||Implications of Amyloid Deposition in Clinically Normal Older Individuals|
- Pittsburgh Compound B (PiB) and F-18 fluorodeoxyglucose (FDG) PET Scan [ Time Frame: at 1 month ] [ Designated as safety issue: No ]
- Cognitive and functional assessments [ Time Frame: Baseline and annually for 5 years ] [ Designated as safety issue: No ]
- Lumbar Puncture (optional) [ Time Frame: Baseline ] [ Designated as safety issue: No ]
|Study Start Date:||November 2008|
|Estimated Study Completion Date:||March 2014|
|Estimated Primary Completion Date:||March 2014 (Final data collection date for primary outcome measure)|
PIB positive, cognitively normal individuals with foci of elevated PIB retention in cortical regions typically affected in AD
PIB negative, cognitively normal individuals without amyloid deposition
There is compelling evidence supporting amyloid as one of the key pathologic agents in AD. Autopsy studies suggest the amount and location of fibrillar amyloid deposition does not relate strongly to the degree and type of clinical impairment, compared to tau pathology and neuronal loss. A substantial percentage of individuals known to be cognitively intact prior to death demonstrate significant amyloid pathology at autopsy. PIB-PET studies of older normal individuals have also demonstrated significant amyloid deposition in substantial percentages.
This study will test the hypothesis that amyloid is associated with synaptic dysfunction and neuronal damage. While some individuals are able to compensate for amyloid-related toxicity for an extended time period, sensitive imaging and neuropsychological markers will reveal that normal subjects with evidence of high amyloid burden do demonstrate evidence of abnormality consistent with prodromal AD.
The study will use a combination of functional, structural, and cognitive measures to detect early effects of amyloid deposition, and will utilize PIB retention in order to characterize the relationship of amyloid to neuropsychological and imaging markers of prodromal AD. The relationship of PIB retention to genetic, plasma and cerebrospinal fluid (CSF) biomarkers will be explored. These preliminary data will be used to determine whether asymptomatic older individuals with high amyloid burden will subsequently manifest cognitive impairment and eventually progress to clinical AD. When completed, this project will either provide evidence that the presence of amyloid deposition is a useful biomarker for incipient AD or raise the possibility that amyloid deposition examined in isolation is insufficient to predict early symptoms and progression of AD.
|United States, Massachusetts|
|Brigham and Women's Hospital||Recruiting|
|Boston, Massachusetts, United States, 02115|
|Contact: Kelly O'Keefe 617-726-6212 email@example.com|
|Contact: Meghan Frey 617-732-8085 firstname.lastname@example.org|
|Principal Investigator: Reisa A. Sperling, MD|
|Sub-Investigator: Keith A. Johnson, MD|
|Principal Investigator:||Reisa Sperling, MD||Director of Clinical Research, Memory Disorders Unit, Brigham and Women's Hospital|