Optimizing protocols for white matter tractography in animal models of genetic AD risk

2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Jacques Andrew Stout ◽  
Robert BJ Anderson ◽  
Gary Cofer ◽  
Carol A Colton ◽  
Alexandra Badea
2007 ◽  
Vol 6 (3) ◽  
pp. 255-266 ◽  
Author(s):  
Anthony M. Choo ◽  
Jie Liu ◽  
Clarrie K. Lam ◽  
Marcel Dvorak ◽  
Wolfram Tetzlaff ◽  
...  

Object In experimental models of spinal cord injury (SCI) researchers have typically focused on contusion and transection injuries. Clinically, however, other injury mechanisms such as fracture–dislocation and distraction also frequently occur. The objective of the present study was to compare the primary damage in three clinically relevant animal models of SCI. Methods Contusion, fracture–dislocation, and flexion–distraction animal models of SCI were developed. To visualize traumatic increases in cellular membrane permeability, fluorescein–dextran was infused into the cerebrospi-nal fluid prior to injury. High-speed injuries (approaching 100 cm/second) were produced in the cervical spine of deeply anesthetized Sprague–Dawley rats (28 SCI and eight sham treated) with a novel multimechanism SCI test system. The animals were killed immediately thereafter so that the authors could characterize the primary injury in the gray and white matter. Sections stained with H & E showed that contusion and dislocation injuries resulted in similar central damage to the gray matter vasculature whereas no overt hemorrhage was detected following distraction. Contusion resulted in membrane disruption of neuronal somata and axons localized within 1 mm of the lesion epicenter. In contrast, membrane compromise in the dislocation and distraction models was observed to extend rostrally up to 5 mm, particularly in the ventral and lateral white matter tracts. Conclusions Given the pivotal nature of hemorrhagic necrosis and plasma membrane compromise in the initiation of downstream SCI pathomechanisms, the aforementioned differences suggest the presence of mechanism-specific injury regions, which may alter future clinical treatment paradigms.


Author(s):  
Jean M Vettel ◽  
Nicole Cooper ◽  
Javier O Garcia ◽  
Fang-Cheng Yeh ◽  
Timothy D Verstynen

2006 ◽  
Vol 25 (8) ◽  
pp. 965-978 ◽  
Author(s):  
O. Friman ◽  
G. Farneback ◽  
C.-F. Westin

2010 ◽  
Vol 78 (1) ◽  
pp. 257-267 ◽  
Author(s):  
Evaggelos Pantelis ◽  
Nikolaos Papadakis ◽  
Kosmas Verigos ◽  
Irene Stathochristopoulou ◽  
Christos Antypas ◽  
...  

2009 ◽  
Vol 15 (1) ◽  
pp. 16-27 ◽  
Author(s):  
M Rausch ◽  
PS Tofts ◽  
P Lervik ◽  
AR Walmsley ◽  
A Mir ◽  
...  

Quantitative magnetization transfer magnetic resonance imaging (qMT-MRI) can be used to improve detection of white matter tissue damage in multiple sclerosis (MS) and animal models thereof. To study the correlation between MT parameters and tissue damage, the magnetization transfer ratio (MTR), the parameter f* (closely related to the bound proton fraction) and the bound proton transverse relaxation time T2B of lesions in a model of focal experimental autoimmune encephalomyelitis (EAE) were measured on a 7T animal scanner and data were compared with histological markers indicative for demyelination, axonal density, and tissue damage. A clear spatial correspondence was observed between reduced values of MTR and demyelination in this animal model. We observed two different levels of MTR and f* reduction for these lesions. One was characterized by a pronounced demyelination and the other corresponded to a more severe loss of the cellular matrix. Changes in f* were generally more pronounced than those of MTR in areas of demyelination. Moreover, a reduction of f* was already observed for tissue where MTR was virtually normal. No changes in T2B were observed for the lesions. We conclude that MTR and qMT mapping are efficient and reliable readouts for studying demyelination in animal models of MS, and that the analysis of regional f* might be even superior to the analysis of MTR values. Therefore, quantitative mapping of f* from human brains might also improve the detection of white matter damage in MS.


NeuroImage ◽  
2006 ◽  
Vol 29 (3) ◽  
pp. 868-878 ◽  
Author(s):  
Paul Thottakara ◽  
Mariana Lazar ◽  
Sterling C. Johnson ◽  
Andrew L. Alexander

2012 ◽  
Vol 32 (8) ◽  
pp. 2773-2782 ◽  
Author(s):  
A. S. Greenberg ◽  
T. Verstynen ◽  
Y.-C. Chiu ◽  
S. Yantis ◽  
W. Schneider ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-17 ◽  
Author(s):  
Hannah C. Kinney ◽  
Joseph J. Volpe

Translational research in preterm brain injury depends upon the delineation of the human neuropathology in order that animal models faithfully reiterate it, thereby ensuring direct relevance to the human condition. The major substrate of human preterm brain injury is the encephalopathy of prematurity that is characterized by gray and white matter lesions reflecting combined acquired insults, altered developmental trajectories, and reparative phenomena. Here we highlight the key features of human preterm brain development and the encephalopathy of prematurity that are critical for modeling in animals. The complete mimicry of the complex human neuropathology is difficult in animal models. Many models focus upon mechanisms related to a specific feature, for example, loss of premyelinating oligodendrocytes in the cerebral white matter. Nevertheless, animal models that simultaneously address oligodendrocyte, neuronal, and axonal injury carry the potential to decipher shared mechanisms and synergistic treatments to ameliorate the global consequences of the encephalopathy of prematurity.


Sign in / Sign up

Export Citation Format

Share Document