Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model
Abstract Background In vivo diffusion tensor imaging (DTI) of the mouse brain was used to identify TDP-43 associated alterations in a mouse model for amyotrophic lateral sclerosis (ALS). Methods Ten mice with TDP-43 G298S overexpression under control of the Thy1.2 promoter and 10 wild type (wt) unde...
| Main Authors: | , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2019-08-01
|
| Series: | Translational Neurodegeneration |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s40035-019-0163-y |
| id |
doaj-438b34fea7024ce1a579b7998b45c10d |
|---|---|
| record_format |
Article |
| spelling |
doaj-438b34fea7024ce1a579b7998b45c10d2020-11-25T03:51:06ZengBMCTranslational Neurodegeneration2047-91582019-08-018111310.1186/s40035-019-0163-yLongitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse modelHans-Peter Müller0David Brenner1Francesco Roselli2Diana Wiesner3Alireza Abaei4Martin Gorges5Karin M. Danzer6Albert C. Ludolph7William Tsao8Philip C. Wong9Volker Rasche10Jochen H. Weishaupt11Jan Kassubek12Department of Neurology, University of UlmDepartment of Neurology, University of UlmDepartment of Neurology, University of UlmDepartment of Neurology, University of UlmCore Facility Small Animal MRI, University of UlmDepartment of Neurology, University of UlmDepartment of Neurology, University of UlmDepartment of Neurology, University of UlmDepartment of Pathology, The Johns Hopkins University School of MedicineDepartment of Pathology, The Johns Hopkins University School of MedicineCore Facility Small Animal MRI, University of UlmDepartment of Neurology, University of UlmDepartment of Neurology, University of UlmAbstract Background In vivo diffusion tensor imaging (DTI) of the mouse brain was used to identify TDP-43 associated alterations in a mouse model for amyotrophic lateral sclerosis (ALS). Methods Ten mice with TDP-43 G298S overexpression under control of the Thy1.2 promoter and 10 wild type (wt) underwent longitudinal DTI scans at 11.7 T, including one baseline and one follow-up scan with an interval of about 5 months. Whole brain-based spatial statistics (WBSS) of DTI-based parameter maps was used to identify longitudinal alterations of TDP-43 G298S mice compared to wt at the cohort level. Results were supplemented by tractwise fractional anisotropy statistics (TFAS) and histological evaluation of motor cortex for signs of neuronal loss. Results Alterations at the cohort level in TDP-43 G298S mice were observed cross-sectionally and longitudinally in motor areas M1/M2 and in transcallosal fibers but not in the corticospinal tract. Neuronal loss in layer V of motor cortex was detected in TDP-43 G298S at the later (but not at the earlier) timepoint compared to wt. Conclusion DTI mapping of TDP-43 G298S mice demonstrated progression in motor areas M1/M2. WBSS and TFAS are useful techniques to localize TDP-43 G298S associated alterations over time in this ALS mouse model, as a biological marker.http://link.springer.com/article/10.1186/s40035-019-0163-yDiffusion tensor imagingAmyotrophic lateral sclerosisMutant TDP-43Fiber trackingMouse brain |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Hans-Peter Müller David Brenner Francesco Roselli Diana Wiesner Alireza Abaei Martin Gorges Karin M. Danzer Albert C. Ludolph William Tsao Philip C. Wong Volker Rasche Jochen H. Weishaupt Jan Kassubek |
| spellingShingle |
Hans-Peter Müller David Brenner Francesco Roselli Diana Wiesner Alireza Abaei Martin Gorges Karin M. Danzer Albert C. Ludolph William Tsao Philip C. Wong Volker Rasche Jochen H. Weishaupt Jan Kassubek Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model Translational Neurodegeneration Diffusion tensor imaging Amyotrophic lateral sclerosis Mutant TDP-43 Fiber tracking Mouse brain |
| author_facet |
Hans-Peter Müller David Brenner Francesco Roselli Diana Wiesner Alireza Abaei Martin Gorges Karin M. Danzer Albert C. Ludolph William Tsao Philip C. Wong Volker Rasche Jochen H. Weishaupt Jan Kassubek |
| author_sort |
Hans-Peter Müller |
| title |
Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model |
| title_short |
Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model |
| title_full |
Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model |
| title_fullStr |
Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model |
| title_full_unstemmed |
Longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the TDP-43 G298S ALS mouse model |
| title_sort |
longitudinal diffusion tensor magnetic resonance imaging analysis at the cohort level reveals disturbed cortical and callosal microstructure with spared corticospinal tract in the tdp-43 g298s als mouse model |
| publisher |
BMC |
| series |
Translational Neurodegeneration |
| issn |
2047-9158 |
| publishDate |
2019-08-01 |
| description |
Abstract Background In vivo diffusion tensor imaging (DTI) of the mouse brain was used to identify TDP-43 associated alterations in a mouse model for amyotrophic lateral sclerosis (ALS). Methods Ten mice with TDP-43 G298S overexpression under control of the Thy1.2 promoter and 10 wild type (wt) underwent longitudinal DTI scans at 11.7 T, including one baseline and one follow-up scan with an interval of about 5 months. Whole brain-based spatial statistics (WBSS) of DTI-based parameter maps was used to identify longitudinal alterations of TDP-43 G298S mice compared to wt at the cohort level. Results were supplemented by tractwise fractional anisotropy statistics (TFAS) and histological evaluation of motor cortex for signs of neuronal loss. Results Alterations at the cohort level in TDP-43 G298S mice were observed cross-sectionally and longitudinally in motor areas M1/M2 and in transcallosal fibers but not in the corticospinal tract. Neuronal loss in layer V of motor cortex was detected in TDP-43 G298S at the later (but not at the earlier) timepoint compared to wt. Conclusion DTI mapping of TDP-43 G298S mice demonstrated progression in motor areas M1/M2. WBSS and TFAS are useful techniques to localize TDP-43 G298S associated alterations over time in this ALS mouse model, as a biological marker. |
| topic |
Diffusion tensor imaging Amyotrophic lateral sclerosis Mutant TDP-43 Fiber tracking Mouse brain |
| url |
http://link.springer.com/article/10.1186/s40035-019-0163-y |
| work_keys_str_mv |
AT hanspetermuller longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT davidbrenner longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT francescoroselli longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT dianawiesner longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT alirezaabaei longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT martingorges longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT karinmdanzer longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT albertcludolph longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT williamtsao longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT philipcwong longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT volkerrasche longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT jochenhweishaupt longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel AT jankassubek longitudinaldiffusiontensormagneticresonanceimaginganalysisatthecohortlevelrevealsdisturbedcorticalandcallosalmicrostructurewithsparedcorticospinaltractinthetdp43g298salsmousemodel |
| _version_ |
1724488810186670080 |