Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition

Increasing evidence demonstrates that there is marked damage and dysfunction not only in the gray matter but also in the white matter in Alzheimer's disease (AD). In this study, transgenic mice overexpressing β-amyloid precursor protein (APP) under control of the platelet-derived growth factor...

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Main Authors: Sheng-Kwei Song, Joong Hee Kim, Shiow-Jiuan Lin, Robert P. Brendza, David M. Holtzman
Format: Article
Language:English
Published: Elsevier 2004-04-01
Series:Neurobiology of Disease
Subjects:
MRI
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996103002687
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record_format Article
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language English
format Article
sources DOAJ
author Sheng-Kwei Song
Joong Hee Kim
Shiow-Jiuan Lin
Robert P. Brendza
David M. Holtzman
spellingShingle Sheng-Kwei Song
Joong Hee Kim
Shiow-Jiuan Lin
Robert P. Brendza
David M. Holtzman
Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
Neurobiology of Disease
Alzheimer's disease
Diffusion tensor
Mice
PDAPP
MRI
Myelin
author_facet Sheng-Kwei Song
Joong Hee Kim
Shiow-Jiuan Lin
Robert P. Brendza
David M. Holtzman
author_sort Sheng-Kwei Song
title Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
title_short Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
title_full Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
title_fullStr Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
title_full_unstemmed Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
title_sort diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
publisher Elsevier
series Neurobiology of Disease
issn 1095-953X
publishDate 2004-04-01
description Increasing evidence demonstrates that there is marked damage and dysfunction not only in the gray matter but also in the white matter in Alzheimer's disease (AD). In this study, transgenic mice overexpressing β-amyloid precursor protein (APP) under control of the platelet-derived growth factor promoter (PDAPP mice) were examined using diffusion tensor magnetic resonance imaging (DTI) to evaluate the extent of white matter injury before and following the development of AD-like pathology. The profile of DTI parameters was significantly different in old PDAPP mice compared to that of old control mice following the development of AD-like pathology. No difference in DTI parameters was observed between the young PDAPP and control mice. Our results suggest that as amyloid β (Aβ) deposition and levels increase over time in PDAPP mice, these changes lead to primary or secondary white matter injury that can be detected by DTI.
topic Alzheimer's disease
Diffusion tensor
Mice
PDAPP
MRI
Myelin
url http://www.sciencedirect.com/science/article/pii/S0969996103002687
work_keys_str_mv AT shengkweisong diffusiontensorimagingdetectsagedependentwhitematterchangesinatransgenicmousemodelwithamyloiddeposition
AT joongheekim diffusiontensorimagingdetectsagedependentwhitematterchangesinatransgenicmousemodelwithamyloiddeposition
AT shiowjiuanlin diffusiontensorimagingdetectsagedependentwhitematterchangesinatransgenicmousemodelwithamyloiddeposition
AT robertpbrendza diffusiontensorimagingdetectsagedependentwhitematterchangesinatransgenicmousemodelwithamyloiddeposition
AT davidmholtzman diffusiontensorimagingdetectsagedependentwhitematterchangesinatransgenicmousemodelwithamyloiddeposition
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spelling doaj-7251f5a456094ab89061963d88adcd6b2021-03-20T04:49:16ZengElsevierNeurobiology of Disease1095-953X2004-04-01153640647Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid depositionSheng-Kwei Song0Joong Hee Kim1Shiow-Jiuan Lin2Robert P. Brendza3David M. Holtzman4Department of Chemistry, Washington University, St. Louis, MO 63130, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Chemistry, Washington University, St. Louis, MO 63130, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Chemistry, Washington University, St. Louis, MO 63130, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Chemistry, Washington University, St. Louis, MO 63130, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USADepartment of Chemistry, Washington University, St. Louis, MO 63130, USA; Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USAIncreasing evidence demonstrates that there is marked damage and dysfunction not only in the gray matter but also in the white matter in Alzheimer's disease (AD). In this study, transgenic mice overexpressing β-amyloid precursor protein (APP) under control of the platelet-derived growth factor promoter (PDAPP mice) were examined using diffusion tensor magnetic resonance imaging (DTI) to evaluate the extent of white matter injury before and following the development of AD-like pathology. The profile of DTI parameters was significantly different in old PDAPP mice compared to that of old control mice following the development of AD-like pathology. No difference in DTI parameters was observed between the young PDAPP and control mice. Our results suggest that as amyloid β (Aβ) deposition and levels increase over time in PDAPP mice, these changes lead to primary or secondary white matter injury that can be detected by DTI.http://www.sciencedirect.com/science/article/pii/S0969996103002687Alzheimer's diseaseDiffusion tensorMicePDAPPMRIMyelin