Amyloid imaging in mild cognitive impairment subtypes
Objective We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome. Methods T...
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| Vydáno v: | Annals of neurology Ročník 65; číslo 5; s. 557 - 568 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.05.2009
Wiley-Liss |
| Témata: | |
| ISSN: | 0364-5134, 1531-8249, 1531-8249 |
| On-line přístup: | Získat plný text |
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| Abstract | Objective
We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome.
Methods
Twenty‐six patients with MCI (13 single‐domain amnestic‐MCI [a‐MCI], 6 multidomain a‐MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty‐three had clinical follow‐up (21.2 ± 16.0 [standard deviation] months) subsequent to their PiB scan.
Results
Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered “amyloid‐positive.” All subtypes were associated with a significant proportion of amyloid‐positive patients (6/13 single‐domain a‐MCI, 5/6 multidomain a‐MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a‐MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid‐positive relative to amyloid‐negative a‐MCI patients. Longitudinal follow‐up demonstrated 5 of 13 amyloid‐positive patients, but 0 of 10 amyloid‐negative patients, converted to clinical AD. Further, 3 of 10 amyloid‐negative patients “reverted to normal.”
Interpretation
These data support the notion that amyloid‐positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease‐specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD. Ann Neurol 2009;65:557–568 |
|---|---|
| AbstractList | We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome.
Twenty-six patients with MCI (13 single-domain amnestic-MCI [a-MCI], 6 multidomain a-MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty-three had clinical follow-up (21.2 +/- 16.0 [standard deviation] months) subsequent to their PiB scan.
Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered "amyloid-positive." All subtypes were associated with a significant proportion of amyloid-positive patients (6/13 single-domain a-MCI, 5/6 multidomain a-MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a-MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid-positive relative to amyloid-negative a-MCI patients. Longitudinal follow-up demonstrated 5 of 13 amyloid-positive patients, but 0 of 10 amyloid-negative patients, converted to clinical AD. Further, 3 of 10 amyloid-negative patients "reverted to normal."
These data support the notion that amyloid-positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease-specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD. Objective We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome. Methods Twenty-six patients with MCI (13 single-domain amnestic-MCI [a-MCI], 6 multidomain a-MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty-three had clinical follow-up (21.2 ± 16.0 [standard deviation] months) subsequent to their PiB scan. Results Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered amyloid-positive. All subtypes were associated with a significant proportion of amyloid-positive patients (6/13 single-domain a-MCI, 5/6 multidomain a-MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a-MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid-positive relative to amyloid-negative a-MCI patients. Longitudinal follow-up demonstrated 5 of 13 amyloid-positive patients, but 0 of 10 amyloid-negative patients, converted to clinical AD. Further, 3 of 10 amyloid-negative patients reverted to normal. Interpretation These data support the notion that amyloid-positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease-specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD. Ann Neurol 2009; 65:557-568. We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome.OBJECTIVEWe utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome.Twenty-six patients with MCI (13 single-domain amnestic-MCI [a-MCI], 6 multidomain a-MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty-three had clinical follow-up (21.2 +/- 16.0 [standard deviation] months) subsequent to their PiB scan.METHODSTwenty-six patients with MCI (13 single-domain amnestic-MCI [a-MCI], 6 multidomain a-MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty-three had clinical follow-up (21.2 +/- 16.0 [standard deviation] months) subsequent to their PiB scan.Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered "amyloid-positive." All subtypes were associated with a significant proportion of amyloid-positive patients (6/13 single-domain a-MCI, 5/6 multidomain a-MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a-MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid-positive relative to amyloid-negative a-MCI patients. Longitudinal follow-up demonstrated 5 of 13 amyloid-positive patients, but 0 of 10 amyloid-negative patients, converted to clinical AD. Further, 3 of 10 amyloid-negative patients "reverted to normal."RESULTSUsing cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered "amyloid-positive." All subtypes were associated with a significant proportion of amyloid-positive patients (6/13 single-domain a-MCI, 5/6 multidomain a-MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a-MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid-positive relative to amyloid-negative a-MCI patients. Longitudinal follow-up demonstrated 5 of 13 amyloid-positive patients, but 0 of 10 amyloid-negative patients, converted to clinical AD. Further, 3 of 10 amyloid-negative patients "reverted to normal."These data support the notion that amyloid-positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease-specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD.INTERPRETATIONThese data support the notion that amyloid-positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease-specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD. Objective We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive impairment (MCI) subtypes and to relate increased PiB binding to other markers of early AD and longitudinal outcome. Methods Twenty‐six patients with MCI (13 single‐domain amnestic‐MCI [a‐MCI], 6 multidomain a‐MCI, and 7 nonamnestic MCI) underwent PiB imaging. Twenty‐three had clinical follow‐up (21.2 ± 16.0 [standard deviation] months) subsequent to their PiB scan. Results Using cutoffs established from a control cohort, we found that 14 (54%) patients had increased levels of PiB retention and were considered “amyloid‐positive.” All subtypes were associated with a significant proportion of amyloid‐positive patients (6/13 single‐domain a‐MCI, 5/6 multidomain a‐MCI, 3/7 nonamnestic MCI). There were no obvious differences in the distribution of PiB retention in the nonamnestic MCI group. Predictors of conversion to clinical AD in a‐MCI, including poorer episodic memory, and medial temporal atrophy, were found in the amyloid‐positive relative to amyloid‐negative a‐MCI patients. Longitudinal follow‐up demonstrated 5 of 13 amyloid‐positive patients, but 0 of 10 amyloid‐negative patients, converted to clinical AD. Further, 3 of 10 amyloid‐negative patients “reverted to normal.” Interpretation These data support the notion that amyloid‐positive patients are likely to have early AD, and that the use of amyloid imaging may have an important role in determining which patients are likely to benefit from disease‐specific therapies. In addition, our data are consistent with longitudinal studies that suggest a significant percentage of all MCI subtypes will develop AD. Ann Neurol 2009;65:557–568 |
| Author | Cohen, Ann D. Saxton, Judy A. Price, Julie C. Aizenstein, Howard J. Wolk, David A. DeKosky, Steven T. Snitz, Beth E. James, Jeffrey A. Weissfeld, Lisa A. Klunk, William E. Lopez, Oscar L. Mathis, Chester A. |
| AuthorAffiliation | 2 Department of Neurology, University of Pittsburgh, Pittsburgh, PA 4 Department of Radiology, University of Pittsburgh, Pittsburgh, PA 1 Alzheimer’s Disease Research Center, University of Pittsburgh, Pittsburgh, PA 5 Department of Biostatistics, University of Pittsburgh, Pittsburgh, PA 3 Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA |
| AuthorAffiliation_xml | – name: 1 Alzheimer’s Disease Research Center, University of Pittsburgh, Pittsburgh, PA – name: 2 Department of Neurology, University of Pittsburgh, Pittsburgh, PA – name: 3 Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA – name: 4 Department of Radiology, University of Pittsburgh, Pittsburgh, PA – name: 5 Department of Biostatistics, University of Pittsburgh, Pittsburgh, PA |
| Author_xml | – sequence: 1 givenname: David A. surname: Wolk fullname: Wolk, David A. email: david.wolk@uphs.upenn.edu organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 2 givenname: Julie C. surname: Price fullname: Price, Julie C. organization: Department of Radiology, University of Pittsburgh, Pittsburgh, PA – sequence: 3 givenname: Judy A. surname: Saxton fullname: Saxton, Judy A. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 4 givenname: Beth E. surname: Snitz fullname: Snitz, Beth E. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 5 givenname: Jeffrey A. surname: James fullname: James, Jeffrey A. organization: Department of Radiology, University of Pittsburgh, Pittsburgh, PA – sequence: 6 givenname: Oscar L. surname: Lopez fullname: Lopez, Oscar L. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 7 givenname: Howard J. surname: Aizenstein fullname: Aizenstein, Howard J. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 8 givenname: Ann D. surname: Cohen fullname: Cohen, Ann D. organization: Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA – sequence: 9 givenname: Lisa A. surname: Weissfeld fullname: Weissfeld, Lisa A. organization: Department of Biostatistics, University of Pittsburgh, Pittsburgh, PA – sequence: 10 givenname: Chester A. surname: Mathis fullname: Mathis, Chester A. organization: Department of Radiology, University of Pittsburgh, Pittsburgh, PA – sequence: 11 givenname: William E. surname: Klunk fullname: Klunk, William E. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA – sequence: 12 givenname: Steven T. surname: DeKosky fullname: DeKosky, Steven T. organization: Alzheimer's Disease Research Center, University of Pittsburgh, Pittsburgh, PA |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21557252$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19475670$$D View this record in MEDLINE/PubMed |
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We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild... We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild cognitive... Objective We utilized the amyloid imaging ligand Pittsburgh Compound B (PiB) to determine the presence of Alzheimer's disease (AD) pathology in different mild... |
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| SubjectTerms | Aged Aged, 80 and over Amyloid - metabolism Aniline Compounds Biological and medical sciences Brain Mapping Cognition Disorders - classification Cognition Disorders - diagnostic imaging Cognition Disorders - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Follow-Up Studies Hippocampus - diagnostic imaging Hippocampus - pathology Humans Magnetic Resonance Imaging - methods Male Medical sciences Middle Aged Neurology Neuropsychological Tests Positron-Emission Tomography - methods Psychometrics - methods Thiazoles |
| Title | Amyloid imaging in mild cognitive impairment subtypes |
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