scholarly journals Effects of melatonin on cognitive impairment and hippocampal neuronal damage in a rat model of chronic cerebral hypoperfusion

2016 ◽  
Vol 11 (6) ◽  
pp. 2240-2246 ◽  
Author(s):  
CHOONG HYUN LEE ◽  
JOON HA PARK ◽  
JI HYEON AHN ◽  
MOO-HO WON
Keyword(s):  
Cognitive Impairment ◽  
Rat Model ◽  
Neuronal Damage ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

scholarly journals Protective Role of S-Nitrosoglutathione (GSNO) Against Cognitive Impairment in Rat Model of Chronic Cerebral Hypoperfusion

2013 ◽  
Vol 34 (3) ◽  
pp. 621-635 ◽  
Author(s):  
Je-Seong Won ◽  
Jinsu Kim ◽  
Balasubramaniam Annamalai ◽  
Anandakumar Shunmugavel ◽  
Inderjit Singh ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Rat Model ◽  
Protective Role ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

Ketamine attenuates hypocapnia-induced neuronal damage in the caudoputamen in a rat model of chronic cerebral hypoperfusion

2004 ◽  
Vol 354 (1) ◽  
pp. 26-29 ◽  
Author(s):  
Etsuko Miyamoto ◽  
Shinichi Nakao ◽  
Hidekazu Tomimoto ◽  
Hideaki Wakita ◽  
Makiko Yamada ◽  
...  
Keyword(s):  
Rat Model ◽  
Neuronal Damage ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

scholarly journals Characterization of Tauopathy in a Rat Model of Post-Stroke Dementia Combining Acute Infarct and Chronic Cerebral Hypoperfusion

2020 ◽  
Vol 21 (18) ◽  
pp. 6929
Author(s):  
Dong Bin Back ◽  
Bo-Ryoung Choi ◽  
Jung-Soo Han ◽  
Kyoung Ja Kwon ◽  
Dong-Hee Choi ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Acute Ischemic Stroke ◽  
Rat Model ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Tau Hyperphosphorylation ◽  
Post Stroke

Post-stroke dementia (PSD) is a major neurodegenerative consequence of stroke. Tauopathy has been reported in diverse neurodegenerative diseases. We investigated the cognitive impairment and pathomechanism associated with tauopathy in a rat model of PSD by modeling acute ischemic stroke and underlying chronic cerebral hypoperfusion (CCH). We performed middle cerebral artery occlusion (MCAO) surgery in rats to mimic acute ischemic stroke, followed by bilateral common carotid artery occlusion (BCCAo) surgery to mimic CCH. We performed behavioral tests and focused on the characterization of tauopathy through histology. Parenchymal infiltration of cerebrospinal fluid (CSF) tracers after intracisternal injection was examined to evaluate glymphatic function. In an animal model of PSD, cognitive impairment was aggravated when BCCAo was combined with MCAO. Tauopathy, manifested by tau hyperphosphorylation, was prominent in the peri-infarct area when CCH was combined. Synergistic accentuation of tauopathy was evident in the white matter. Microtubules in the neuronal axon and myelin sheath showed partial colocalization with the hyperphosphorylated tau, whereas oligodendrocytes showed near-complete colocalization. Parenchymal infiltration of CSF tracers was attenuated in the PSD model. Our experimental results suggest a hypothesis that CCH may aggravate cognitive impairment and tau hyperphosphorylation in a rat model of PSD by interfering with tau clearance through the glymphatic system. Therapeutic strategies to improve the clearance of brain metabolic wastes, including tau, may be a promising approach to prevent PSD after stroke.

Abstract WP156: Characterization of Tauopathy in a Rat Model of Post-Stroke Dementia Combining Acute Infarct and Chronic Cerebral Hypoperfusion

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Hahn Young Kim ◽  
Pil-Wook Chung
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Acute Ischemic Stroke ◽  
Rat Model ◽  
Artery Occlusion ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Tau Hyperphosphorylation ◽  
Post Stroke

Post-stroke dementia (PSD) is a major neurodegenerative consequence of stroke. Tauopathy has been reported in diverse neurodegenerative diseases. We investigated cognitive impairments and pathomechanisms of tauopathy in a rat model of PSD by modeling acute ischemic stroke and underlying chronic cerebral hypoperfusion (CCH) in the same animal. We performed middle cerebral artery occlusion (MCAO) surgery in rats, to mimic acute ischemic stroke, followed by bilateral common carotid artery occlusion (BCCAo) surgery, to mimic CCH. We performed behavioral tests and focused on the characterization of tauopathy through histology. Parenchymal infiltration of cerebrospinal fluid (CSF) tracers after intracisternal injection was examined to evaluate glymphatic clearance. In an animal model of PSD, cognitive impairment was aggravated when BCCAo was superimposed on MCAO. Tauopathy, manifested by tau hyperphosphorylation, was prominent in the penumbra when CCH was combined with acute ischemic stroke. Synergistic accentuation of tauopathy was more evident in the white matter. Oligodendrocytes and some neurons were colocalized with tau hyperphosphorylation. Parenchymal infiltration of CSF tracers was attenuated in the PSD model. Our experimental results suggest that CCH may aggravate cognitive impairment and tau hyperphosphorylation in a rat model of PSD by interfering with tau clearance through glymphatic pathway. Therapeutic strategies to improve clearance of brain metabolic wastes, including tau, may be a promising approach to prevent PSD after stroke.

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