Abstract
The purpose of this study was to evaluate the capacity of [{sup 11}C]6-OH-BTA-1 and positron emission tomography (PET) to quantify {beta}-amyloid (A{beta}) plaques in the Tg2576 mouse model of Alzheimer's disease (AD). PET imaging was performed with the NIH ATLAS small animal scanner in six elderly transgenic mice (Tg2576; age 22.0{+-}1.8 months; 23.6{+-}2.6 g) overexpressing a mutated form of human {beta}-amyloid precursor protein (APP) known to result in the production of A{beta} plaques, and in six elderly wild-type litter mates (age 21.8{+-}1.6 months; 29.5{+-}4.7 g). Dynamic PET scans were performed for 30 min in each mouse under 1% isoflurane inhalation anesthesia after a bolus injection of 13-46 MBq of [{sup 11}C]6-OH-BTA-1. PET data were reconstructed with 3D OSEM. On the coronal PET image, irregular regions of interest (ROIs) were placed on frontal cortex (FR), parietal cortex (PA), striatum (ST), thalamus (TH), pons (PO), and cerebellum (CE), guided by a mouse stereotaxic atlas. Time-activity curves (TACs) (expressed as percent injected dose per gram normalized to body weight: % ID-kg/g) were obtained for FR, PA, ST, TH, PO, and CE. ROI-to-CE radioactivity ratios were also calculated. Following PET scans, sections of mouse brain prepared from anesthetized and fixative-perfused mice were stained with
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Toyama, Hiroshi;
[1]
National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)];
Ye, Daniel;
Cohen, Robert M;
[2]
Ichise, Masanori;
Liow, Jeih-San;
Cai, Lisheng;
Musachio, John L;
Hong, Jinsoo;
Crescenzo, Mathew;
Tipre, Dnyanesh;
Lu, Jian-Qiang;
Zoghbi, Sami;
Vines, Douglass C;
Pike, Victor W;
Innis, Robert B;
[3]
Jacobowitz, David;
[4]
Seidel, Jurgen;
Green, Michael V;
[5]
Katada, Kazuhiro
[1]
- Fujita Health University, Department of Radiology, Aichi (Japan)
- National Institutes of Health, Geriatric Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland (United States)
- National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)
- USUHS, Department of Anatomy, Physiology, and Genetics, Bethesda, Maryland (United States)
- National Institutes of Health, Department of Nuclear Medicine, Warren Grant Magnuson Clinical Center, Bethesda, Maryland (United States)
Citation Formats
Toyama, Hiroshi, National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)], Ye, Daniel, Cohen, Robert M, Ichise, Masanori, Liow, Jeih-San, Cai, Lisheng, Musachio, John L, Hong, Jinsoo, Crescenzo, Mathew, Tipre, Dnyanesh, Lu, Jian-Qiang, Zoghbi, Sami, Vines, Douglass C, Pike, Victor W, Innis, Robert B, Jacobowitz, David, Seidel, Jurgen, Green, Michael V, and Katada, Kazuhiro.
PET imaging of brain with the {beta}-amyloid probe, [{sup 11}C]6-OH-BTA-1, in a transgenic mouse model of Alzheimer's disease.
Germany: N. p.,
2005.
Web.
doi:10.1007/s00259-005-1780-5.
Toyama, Hiroshi, National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)], Ye, Daniel, Cohen, Robert M, Ichise, Masanori, Liow, Jeih-San, Cai, Lisheng, Musachio, John L, Hong, Jinsoo, Crescenzo, Mathew, Tipre, Dnyanesh, Lu, Jian-Qiang, Zoghbi, Sami, Vines, Douglass C, Pike, Victor W, Innis, Robert B, Jacobowitz, David, Seidel, Jurgen, Green, Michael V, & Katada, Kazuhiro.
PET imaging of brain with the {beta}-amyloid probe, [{sup 11}C]6-OH-BTA-1, in a transgenic mouse model of Alzheimer's disease.
Germany.
https://doi.org/10.1007/s00259-005-1780-5
Toyama, Hiroshi, National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)], Ye, Daniel, Cohen, Robert M, Ichise, Masanori, Liow, Jeih-San, Cai, Lisheng, Musachio, John L, Hong, Jinsoo, Crescenzo, Mathew, Tipre, Dnyanesh, Lu, Jian-Qiang, Zoghbi, Sami, Vines, Douglass C, Pike, Victor W, Innis, Robert B, Jacobowitz, David, Seidel, Jurgen, Green, Michael V, and Katada, Kazuhiro.
2005.
"PET imaging of brain with the {beta}-amyloid probe, [{sup 11}C]6-OH-BTA-1, in a transgenic mouse model of Alzheimer's disease."
Germany.
https://doi.org/10.1007/s00259-005-1780-5.
@misc{etde_20604515,
title = {PET imaging of brain with the {beta}-amyloid probe, [{sup 11}C]6-OH-BTA-1, in a transgenic mouse model of Alzheimer's disease}
author = {Toyama, Hiroshi, National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)], Ye, Daniel, Cohen, Robert M, Ichise, Masanori, Liow, Jeih-San, Cai, Lisheng, Musachio, John L, Hong, Jinsoo, Crescenzo, Mathew, Tipre, Dnyanesh, Lu, Jian-Qiang, Zoghbi, Sami, Vines, Douglass C, Pike, Victor W, Innis, Robert B, Jacobowitz, David, Seidel, Jurgen, Green, Michael V, and Katada, Kazuhiro}
abstractNote = {The purpose of this study was to evaluate the capacity of [{sup 11}C]6-OH-BTA-1 and positron emission tomography (PET) to quantify {beta}-amyloid (A{beta}) plaques in the Tg2576 mouse model of Alzheimer's disease (AD). PET imaging was performed with the NIH ATLAS small animal scanner in six elderly transgenic mice (Tg2576; age 22.0{+-}1.8 months; 23.6{+-}2.6 g) overexpressing a mutated form of human {beta}-amyloid precursor protein (APP) known to result in the production of A{beta} plaques, and in six elderly wild-type litter mates (age 21.8{+-}1.6 months; 29.5{+-}4.7 g). Dynamic PET scans were performed for 30 min in each mouse under 1% isoflurane inhalation anesthesia after a bolus injection of 13-46 MBq of [{sup 11}C]6-OH-BTA-1. PET data were reconstructed with 3D OSEM. On the coronal PET image, irregular regions of interest (ROIs) were placed on frontal cortex (FR), parietal cortex (PA), striatum (ST), thalamus (TH), pons (PO), and cerebellum (CE), guided by a mouse stereotaxic atlas. Time-activity curves (TACs) (expressed as percent injected dose per gram normalized to body weight: % ID-kg/g) were obtained for FR, PA, ST, TH, PO, and CE. ROI-to-CE radioactivity ratios were also calculated. Following PET scans, sections of mouse brain prepared from anesthetized and fixative-perfused mice were stained with thioflavin-S. TACs for [{sup 11}C]6-OH-BTA-1 in all ROIs peaked early (at 30-55 s), with radioactivity washing out quickly thereafter in both transgenic and wild-type mice. Peak uptake in all regions was significantly lower in transgenic mice than in wild-type mice. During the later part of the washout phase (12-30 min), the mean FR/CE and PA/CE ratios were higher in transgenic than in wild-type mice (1.06{+-}0.04 vs 0.98{+-}0.07, p=0.04; 1.06{+-}0.09 vs 0.93{+-}0.08 p=0.02) while ST/CE, TH/CE, and PO/CE ratios were not. Ex vivo staining revealed widespread A{beta} plaques in cortex, but not in cerebellum of transgenic mice or in any brain regions of wild-type mice. Marked reductions in brain uptake of this radioligand in transgenic mice may be due to reduced cerebral blood flow relative to that in wild-type mice. (orig.)}
doi = {10.1007/s00259-005-1780-5}
journal = []
issue = {5}
volume = {32}
journal type = {AC}
place = {Germany}
year = {2005}
month = {Apr}
}
title = {PET imaging of brain with the {beta}-amyloid probe, [{sup 11}C]6-OH-BTA-1, in a transgenic mouse model of Alzheimer's disease}
author = {Toyama, Hiroshi, National Institutes of Health, Molecular Imaging Branch, National Institute of Mental Health, Bethesda, Maryland (United States)], Ye, Daniel, Cohen, Robert M, Ichise, Masanori, Liow, Jeih-San, Cai, Lisheng, Musachio, John L, Hong, Jinsoo, Crescenzo, Mathew, Tipre, Dnyanesh, Lu, Jian-Qiang, Zoghbi, Sami, Vines, Douglass C, Pike, Victor W, Innis, Robert B, Jacobowitz, David, Seidel, Jurgen, Green, Michael V, and Katada, Kazuhiro}
abstractNote = {The purpose of this study was to evaluate the capacity of [{sup 11}C]6-OH-BTA-1 and positron emission tomography (PET) to quantify {beta}-amyloid (A{beta}) plaques in the Tg2576 mouse model of Alzheimer's disease (AD). PET imaging was performed with the NIH ATLAS small animal scanner in six elderly transgenic mice (Tg2576; age 22.0{+-}1.8 months; 23.6{+-}2.6 g) overexpressing a mutated form of human {beta}-amyloid precursor protein (APP) known to result in the production of A{beta} plaques, and in six elderly wild-type litter mates (age 21.8{+-}1.6 months; 29.5{+-}4.7 g). Dynamic PET scans were performed for 30 min in each mouse under 1% isoflurane inhalation anesthesia after a bolus injection of 13-46 MBq of [{sup 11}C]6-OH-BTA-1. PET data were reconstructed with 3D OSEM. On the coronal PET image, irregular regions of interest (ROIs) were placed on frontal cortex (FR), parietal cortex (PA), striatum (ST), thalamus (TH), pons (PO), and cerebellum (CE), guided by a mouse stereotaxic atlas. Time-activity curves (TACs) (expressed as percent injected dose per gram normalized to body weight: % ID-kg/g) were obtained for FR, PA, ST, TH, PO, and CE. ROI-to-CE radioactivity ratios were also calculated. Following PET scans, sections of mouse brain prepared from anesthetized and fixative-perfused mice were stained with thioflavin-S. TACs for [{sup 11}C]6-OH-BTA-1 in all ROIs peaked early (at 30-55 s), with radioactivity washing out quickly thereafter in both transgenic and wild-type mice. Peak uptake in all regions was significantly lower in transgenic mice than in wild-type mice. During the later part of the washout phase (12-30 min), the mean FR/CE and PA/CE ratios were higher in transgenic than in wild-type mice (1.06{+-}0.04 vs 0.98{+-}0.07, p=0.04; 1.06{+-}0.09 vs 0.93{+-}0.08 p=0.02) while ST/CE, TH/CE, and PO/CE ratios were not. Ex vivo staining revealed widespread A{beta} plaques in cortex, but not in cerebellum of transgenic mice or in any brain regions of wild-type mice. Marked reductions in brain uptake of this radioligand in transgenic mice may be due to reduced cerebral blood flow relative to that in wild-type mice. (orig.)}
doi = {10.1007/s00259-005-1780-5}
journal = []
issue = {5}
volume = {32}
journal type = {AC}
place = {Germany}
year = {2005}
month = {Apr}
}