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Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

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Author(s)
Bo-Ryoung ChoiSang Rim LeeJung-Soo HanSang-Keun WooKyeong Min KimDong-Hee ChoiKyoung Ja KwonSeol-Heui HanChan Young ShinJongmin LeeChin-Sang ChungSeong-Ryong LeeHahn Young Kim
Keimyung Author(s)
Lee, Seong Ryong
Department
Dept. of Pharmacology (약리학)
Brain Research Institute (뇌연구소)
Journal Title
Stroke
Issued Date
2011
Volume
42
Issue
9
Keyword
Alzheimer diseaseamyloid betachronic cerebral hypoperfusionMorris water mazevascular dementia
Abstract
Background and Purpose: Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (Aβ) toxicity.
Methods: In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular Aβ (Aβ toxicity) using a nonphysiological Aβ peptide (Aβ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (Aβ toxicity or BCCAo), and combined injury (BCCAo-Aβ toxicity) groups (n=7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed.
Results: Spatial memory impairment was synergistically exacerbated in the BCCAo–Aβ toxicity group as compared to the BCCAo or Aβ toxicity groups (P<0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo–Aβ toxicity group compared to the Aβ toxicity group.
Conclusion: Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebral hypoperfusion and Aβ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury.
Keimyung Author(s)(Kor)
이성용
Publisher
School of Medicine
Citation
Bo-Ryoung Choi et al. (2011). Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model. Stroke, 42(9), 2595–2604. doi: 10.1161/STROKEAHA.111.620179
Type
Article
ISSN
0039-2499
DOI
10.1161/STROKEAHA.111.620179
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34425
Appears in Collections:
3. Research Institutues (연구소) > Brain Research Institute (뇌연구소)
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
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