Practice Effects and Amyloid Imaging Using 18F-PIB or Flutemetamol PET and FDG-PET
| Status: | Active, not recruiting |
|---|---|
| Conditions: | Alzheimer Disease |
| Therapuetic Areas: | Neurology |
| Healthy: | No |
| Age Range: | 65 - Any |
| Updated: | 2/9/2018 |
| Start Date: | May 2011 |
| End Date: | December 2018 |
Practice Effects and Amyloid Imaging Using 18F-PIB (18F-39-F-6-OH-BTA1) Known as [18FGE067]) or Flutemetamol PET and FDG-PET
Alzheimer's disease (AD) is the most common cause of progressive cognitive decline in the
United States. AD is characterized by severe impairments in learning, memory and other
cognitive abilities that significantly interfere with daily functioning. The neuropathologic
hallmarks of AD consist of neuritic plaques, neurofibrillary tangles, and selective neuronal
cell loss. Amyloid plaques, which contain Abeta protein, are believed to play an integral
role in the development of AD. Elevated levels of Abeta in the brain are also correlated with
cognitive decline.
Alzheimer's (AD) develops insidiously, making it difficult to identify early, yet treatment
is most effective when begun during the early stages of the disease. Thus, it has become
important for researchers to identify markers of early AD. This project will examine the
relationship between four potential markers that may indicate the early development of AD:
1. Mild cognitive impairment (MCI)or normal cognition
2. Practice effects
3. Amyloid plaque binding on 18F-PIB PET
4. Glucose hypometabolism on FDG PET
This project will recruit 25 subjects from an ongoing community-based study of memory and
practice effects in cognitively normal, community-dwelling individuals who are age 65 and
over (NIA #5K23AG028417-05). Each subject will undergo positron emission tomography (PET)
with both 18F-Flutemetamol and FDG.
The overall objective of this companion project is to study the biodistribution and binding
of 18F-Flutemetamol in these subjects using PET imaging, which will provide biological
evidence to support the overall hypothesis that failure to benefit from practice on a
learning paradigm is an early marker of AD.
United States. AD is characterized by severe impairments in learning, memory and other
cognitive abilities that significantly interfere with daily functioning. The neuropathologic
hallmarks of AD consist of neuritic plaques, neurofibrillary tangles, and selective neuronal
cell loss. Amyloid plaques, which contain Abeta protein, are believed to play an integral
role in the development of AD. Elevated levels of Abeta in the brain are also correlated with
cognitive decline.
Alzheimer's (AD) develops insidiously, making it difficult to identify early, yet treatment
is most effective when begun during the early stages of the disease. Thus, it has become
important for researchers to identify markers of early AD. This project will examine the
relationship between four potential markers that may indicate the early development of AD:
1. Mild cognitive impairment (MCI)or normal cognition
2. Practice effects
3. Amyloid plaque binding on 18F-PIB PET
4. Glucose hypometabolism on FDG PET
This project will recruit 25 subjects from an ongoing community-based study of memory and
practice effects in cognitively normal, community-dwelling individuals who are age 65 and
over (NIA #5K23AG028417-05). Each subject will undergo positron emission tomography (PET)
with both 18F-Flutemetamol and FDG.
The overall objective of this companion project is to study the biodistribution and binding
of 18F-Flutemetamol in these subjects using PET imaging, which will provide biological
evidence to support the overall hypothesis that failure to benefit from practice on a
learning paradigm is an early marker of AD.
The overall objective of this companion study project is to study the biodistribution and
binding of 18F-Flutemetamol using PET imaging in community-dwelling functionally intact
elderly subjects. Understanding the biodistribution and binding of this radiopharmaceutical
in normal patients with various levels of potential for cognitive decline will help determine
its appropriate role as a disease biomarker and aid in the interpretation of images produced
with this agent. Comparison with FDG-PET is essential to correlate metabolic changes and for
anatomic co-registration of 18F-PIB images necessary for group analysis.
We will use 18F-Flutemetamol and FDG-PET to compare subjects with low and high practice
effects with the following aims and hypotheses:
Specific Aim 1: Examine the relationship between practice effects and amyloid burden in a
community sample.
Specific Aim 2: Determine whether FDG-PET or 18F-Flutemetamol better distinguish individuals
with high and low practice effects.
Hypothesis 1: Practice effects will be negatively correlated with amyloid deposition, so that
higher levels of practice effects (i.e., better repeat testing) will be associated with lower
levels of brain amyloid deposition and lower levels of practice effects (i.e., poorer repeat
testing) will be associated with greater levels of brain amyloid and these two groups are
more clearly distinguishable with 18F-PIB than FDG-PET.
Hypothesis 2: Patients with increased amyloid deposition shown with 18F-PIB will have an
FDG-PET scan with more pronounced temporal and parietal hypometabolism as noted on visual
review of images and on statistical image analysis.
binding of 18F-Flutemetamol using PET imaging in community-dwelling functionally intact
elderly subjects. Understanding the biodistribution and binding of this radiopharmaceutical
in normal patients with various levels of potential for cognitive decline will help determine
its appropriate role as a disease biomarker and aid in the interpretation of images produced
with this agent. Comparison with FDG-PET is essential to correlate metabolic changes and for
anatomic co-registration of 18F-PIB images necessary for group analysis.
We will use 18F-Flutemetamol and FDG-PET to compare subjects with low and high practice
effects with the following aims and hypotheses:
Specific Aim 1: Examine the relationship between practice effects and amyloid burden in a
community sample.
Specific Aim 2: Determine whether FDG-PET or 18F-Flutemetamol better distinguish individuals
with high and low practice effects.
Hypothesis 1: Practice effects will be negatively correlated with amyloid deposition, so that
higher levels of practice effects (i.e., better repeat testing) will be associated with lower
levels of brain amyloid deposition and lower levels of practice effects (i.e., poorer repeat
testing) will be associated with greater levels of brain amyloid and these two groups are
more clearly distinguishable with 18F-PIB than FDG-PET.
Hypothesis 2: Patients with increased amyloid deposition shown with 18F-PIB will have an
FDG-PET scan with more pronounced temporal and parietal hypometabolism as noted on visual
review of images and on statistical image analysis.
Inclusion Criteria:
- Subjects must be currently enrolled in an NIA-sponsored, community-based study of
practice effects in non-demented adults age 65 and older living independently (NIA
#5K23AG028417-05)
Exclusion Criteria:
- History of neurological disease known to affect cognition (e.g., stroke, head injury
with loss of consciousness of >30 minutes, seizure disorder, demyelinating disorder,
mental retardation, etc.)
- Dementia based on DSM-IV criteria
- Current or past major psychiatric illness (e.g., schizophrenia, bipolar affective
disorder)
- 30-item Geriatric Depression Score >14
- Evidence of stroke or mass lesion on CT or MRI scan
- History of alcoholism or other substance abuse
- Current use of cholinesterase inhibitors, other cognitive enhancers, antipsychotics,
or anticonvulsant medications
- History of radiation therapy to the brain
- History of significant major medical illnesses, such as cancer or AIDS
- Uncontrolled diabetes or blood glucose >180 mg/dl on the day of the FDG-PET scan
- Currently pregnant
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