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| Sponsor: | University of Utah |
|---|---|
| Information provided by: | University of Utah |
| ClinicalTrials.gov Identifier: | NCT00811122 |
Purpose
Alzheimer's disease is characterized by neuritic plaques, neurofibrillary tangles, and neuronal cell loss. Amyloid plaques are believed to play an integral role in AD. Elevated levels of Aβ in the brain are correlated with cognitive decline.
There are no approved ways to measure amyloid load in humans. Several compounds are under investigation. All of these compounds use radioactive chemical tags for PET imaging. The most promising compound is 11C-PIB, or Pittsburgh Compound-B. This compound can be injected, and a PET scan performed. This allows doctors to see the amyloid plaques in the brain, and to use this information to look at other types of dementia to see if there are differences and/or similarities in the plaques.
We will recruit a total of 30 subjects, 10 from each of the following 3 diagnostic categories: frontal temporal dementia, Alzheimer's disease, normal volunteers. All subjects will be given an FDG-PET scan (if they haven't had one in the past) and a PIB-PET scan.
The overall objective of this project is to study the biodistribution of 11C-PIB using PET imaging in normal elderly volunteers and relevant patient groups.
| Condition | Intervention | Phase |
|---|---|---|
|
Alzheimer's Disease |
Other: 11-C PIB |
Phase II |
| Study Type: | Interventional |
| Study Design: | Allocation: Non-Randomized Endpoint Classification: Bio-availability Study Intervention Model: Single Group Assignment Masking: Open Label Primary Purpose: Basic Science |
| Official Title: | Biodistribution of 11C-PIB PET in Alzheimer's Disease, Frontotemporal Dementia, and Cognitively Normal Elderly |
| Estimated Enrollment: | 30 |
| Study Start Date: | November 2009 |
| Estimated Study Completion Date: | December 2011 |
| Estimated Primary Completion Date: | June 2011 (Final data collection date for primary outcome measure) |
| Arms | Assigned Interventions |
|---|---|
|
PET Scan
10 patients with AD, 10 patients with FTD, and 10 normal patients will be getting a PIB PET scan and an FDG PET scan if they haven't had one in the past.
|
Other: 11-C PIB
300MBq of PIB will be used for each subject. C-11 PIB ( [11C] 6-OH-BTA-1 Injection) will be produced by the Cyclotron Radiochemistry Laboratory at the Huntsman Cancer Institute (HCI) and its staff of radiochemists and radiopharmacist. The processes used for the production of 11C-PIB will be performed in the same manner as F-18 FDG, F-18 FLT, N-13 ammonia, O-15 water and other materials that would be produced for PET imaging in humans. The laboratory uses Good Manufacturing Practices (GMP) as guidance documents under the license of the State of Utah for radiopharmaceutical manufacturing. Other Name: PIB
|
Biomarkers of Alzheimer's disease (AD) have recently become extremely important for a number of reasons: to improve diagnosis, to measure severity of disease, to measure progression of disease, to measure effects of novel disease-modifying drugs and to speed development of these novel experimental drugs by reducing time needed to follow patients, number of patients to be followed per study, and cost of research. (Thal, 2006, Nichols, 2006)
The neuropathology of AD is characterized by neuritic plaques, neurofibrillary tangles, and neuronal cell loss. (Braak and Braak 1997) Amyloid plaques are believed to play an integral role in AD. (Selkoe, 1993) Plaques are neurotoxic. (Yankner, 1989) Elevated levels of Aβ in the brain are correlated with cognitive decline. (Naslund, 2000) Removal of plaques in animal models of AD results in behavioral improvements. (Arendash, 2001)
There are no approved in vivo markers of amyloid load in humans. Several compounds with affinity for binding amyloid in vivo are under investigation. All of these compounds use radioactive chemical tags for PET imaging. Attempts at finding non-radioactive amyloid tracers are underway, but still poorly developed. The most promising compound is 11C-PIB. Pittsburgh Compound-B has statistically significant increased retention in AD cortical areas, relative to controls (P<0.05). (Price, 2005) To our knowledge, 11C-PIB imaging has not been compared against FTD controls.
We will recruit (from our clinic population), a total of 30 subjects, 10 from each of the following 3 diagnostic categories: frontal temporal dementia, Alzheimer's disease, normal volunteers. All subjects will be given an FDG-PET scan (if they haven't had one in the past) and a PIB-PET scan.
Objective and Hypothesis:
The overall objective of this project is to study the biodistribution of 11C-PIB using PET imaging in normal elderly volunteers and relevant patient groups. Comparison with FDG-PET is essential to confirm group membership and for anatomic co-registration of 11C-PIB images.
Specific Aim 1: Determine the biodistribution of 11C-PIB in AD, FTD, and cognitively normal elderly individuals and determine whether it reflects the distribution of amyloid plaques in the brain expected from postmortem studies.
Hypothesis 1: The agent 11C-PIB has similar biodistribution outside the brain in AD, FTD, and cognitively normal elderly individuals.
Hypothesis 2: Patients with AD scanned with 11C-PIB will have higher standardized uptake values (SUVs) than cognitively normal elderly in brain regions where beta amyloid are expected to be over-expressed.
Hypothesis 3: Patients with FTD scanned with 11C-PIB will have similar standardized uptake values (SUVs) as cognitively normal elderly subjects and lower values than in AD subjects in brain regions where beta amyloid are expected in AD to be overexpressed.
Specific Aim 2: Correlate glucose metabolism with 11C-PIB PET results.
Hypothesis 4: Patients with a pattern of glucose hypometabolism suggestive of FTD with FDG-PET have 11C-PIB uptake and brain biodistribution similar to cognitively normal elderly, while those with a pattern of glucose hypometabolism suggestive of AD have abnormal PIB uptake and brain biodistribution of 11C-PIB
Eligibility| Ages Eligible for Study: | 30 Years to 90 Years |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | Yes |
Inclusion Criteria:
General inclusion criteria are shown below:
Exclusion Criteria:
Contacts and Locations| United States, Utah | |
| University of Utah Center for Alzheimer's Care, Imaging and Research | |
| Salt Lake City, Utah, United States, 84108 | |
| Principal Investigator: | Norman L Foster, MD | University of Utah Center for Alzheimer's Care, Imaging and Research |
More Information
| Responsible Party: | John Hoffman, MD, University of Utah Medical Center / Huntsman Cancer Institute |
| ClinicalTrials.gov Identifier: | NCT00811122 History of Changes |
| Other Study ID Numbers: | 17991 |
| Study First Received: | December 16, 2008 |
| Last Updated: | May 6, 2011 |
| Health Authority: | United States: Food and Drug Administration |
|
Alzheimer's disease frontal temporal dementia |
|
Alzheimer Disease Dementia Frontotemporal Dementia Aphasia, Primary Progressive Pick Disease of the Brain Brain Diseases Central Nervous System Diseases Nervous System Diseases Tauopathies Neurodegenerative Diseases Delirium, Dementia, Amnestic, Cognitive Disorders Mental Disorders |
Frontotemporal Lobar Degeneration TDP-43 Proteinopathies Proteostasis Deficiencies Metabolic Diseases Aphasia Speech Disorders Language Disorders Communication Disorders Neurobehavioral Manifestations Neurologic Manifestations Signs and Symptoms |
