Characterization of White Matter Injury in a Rat Model of Chronic Cerebral Hypoperfusion

Autor: Dong-Hee Choi, Bo-Ryoung Choi, Dong-Hee Kim, Dong Bin Back, Bo-Ram Kim, Chan Young Shin, Jung-Soo Han, Kyoung Ja Kwon, Chung Hwan Kang, Won-Jin Moon, Jongmin Lee, Hahn Young Kim, Seol-Heui Han
Rok vydání: 2016
Předmět:
0301 basic medicine
Pathology
medicine.medical_specialty
Tetrazoles
Water maze
Neuropsychological Tests
Hippocampus
Brain Ischemia
Brain ischemia
White matter
03 medical and health sciences
Myelin
Cognition
0302 clinical medicine
Leukoencephalopathies
Ranvier's Nodes
medicine
Animals
Carotid Stenosis
Rats
Wistar
Vascular dementia
Neuroinflammation
Inflammation
Advanced and Specialized Nursing
Behavior
Animal
biology
business.industry
Dementia
Vascular
Myelin Basic Protein
medicine.disease
White Matter
Cilostazol
Rats
Myelin basic protein
Disease Models
Animal
Oligodendroglia
Diffusion Tensor Imaging
Neuroprotective Agents
030104 developmental biology
medicine.anatomical_structure
Chronic Disease
biology.protein
Neurology (clinical)
Cardiology and Cardiovascular Medicine
business
030217 neurology & neurosurgery
Diffusion MRI
Zdroj: Stroke. 47:542-547
ISSN: 1524-4628
0039-2499
Popis: Background and Purpose— Chronic cerebral hypoperfusion can lead to ischemic white matter injury resulting in vascular dementia. To characterize white matter injury in vascular dementia, we investigated disintegration of diverse white matter components using a rat model of chronic cerebral hypoperfusion. Methods— Chronic cerebral hypoperfusion was modeled in Wistar rats by permanent occlusion of the bilateral common carotid arteries. We performed cognitive behavioral tests, including the water maze task, odor discrimination task, and novel object test; histological investigation of neuroinflammation, oligodendrocytes, myelin basic protein, and nodal or paranodal proteins at the nodes of Ranvier; and serial diffusion tensor imaging. Cilostazol was administered to protect against white matter injury. Results— Diverse cognitive impairments were induced by chronic cerebral hypoperfusion. Disintegration of white matter was characterized by neuroinflammation, loss of oligodendrocytes, attenuation of myelin density, structural derangement at the nodes of Ranvier, and disintegration of white matter tracts. Cilostazol protected against cognitive impairments and white matter disintegration. Conclusions— White matter injury induced by chronic cerebral hypoperfusion can be characterized by disintegration of diverse white matter components. Cilostazol might be a therapeutic strategy against white matter disintegration in patients with vascular dementia.
Databáze: OpenAIRE
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