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The related main theme: A. Stroke and Cerebral vascular disorders

α-硫辛酸通過調節糖原合成酶激酶-3β在短暫性中大腦動脈阻塞的大鼠模型中減輕腦缺血性損傷引起的認知障礙與阿茲海默氏病樣病理

Alpha-Lipoic acid alleviates cerebral ischemic injury-induced cognitive impairment and Alzheimer’s Disease-like pathologies through modulation of GSK-3β in a rat model of transient middle cerebral artery occlusion

Authers:

吳明修, PhD, MD 1, 2 , 張嘉祐, PhD, MD  , 
Wu  Ming-Hsiu, PhD, MD 1, 2 , Chang  Chia- Yu , PhD, MD  , 
1 柳營奇美醫院神經內科, 台南, 台灣
2 敏惠醫護管理專科學校長期照顧與健康促進管理科, 台南, 台灣
1 Division of Neurology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan;
2 Department of Long-Term Care and Health Promotion, Min-Hwei Junior College of Health Care Management, Tainan, Taiwan
Corresponding Author:

吳明修
Wu  Ming-Hsiu , PhD, MD
柳營奇美醫院神經內科, 台南, 台灣; 敏惠醫護管理專科學校長期照顧與健康促進管理科, 台南, 台灣
Division of Neurology, Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan; Department of Long-Term Care and Health Promotion, Min-Hwei Junior College of Health Care Management, Tainan, Taiwan

keywords: dementia, vascular cognitive impairment and dementia (VCID), cerebral ischemia-reperfusion (I/R) injury, alpha-lipoic acid (ALA), glycogen synthase kinase-3β (GSK-3β)
Abstract for original article

OBJECTIVES /BACKGROUND:
Dementia is composed of mainly two subtypes: Alzheimer’s disease (AD) and vascular cognitive impairment and dementia (VCID). Alpha-lipoic acid (ALA) has properties of anti-oxidation and anti-inflammation, and is protective against cerebral ischemia-reperfusion (I/R) injury. We aimed to investigate the protective role of ALA in cerebral I/R injury-related cognitive impairment in a rat model of transient middle cerebral artery occlusion (tMCAO), which mimics VCID in humans.

MATERIAL and METHOD:
The rats after I/R injury were treated with either intraperitoneal injection of ALA, 25 mg/kg, or vehicle. Infarction volume, brain edema, modified neurologic severity scores (mNSS) and Y Maze Test for cognitive impairment were assessed. In addition, activation of glycogen synthase kinase-3β (GSK-3β) and microglia, and expressions of amyloid-β precursor protein (APP), β-site APP cleaving enzyme 1 (BACE1), amyloid-β (Aβ), tau and synaptophysin were measured 7 days after tMCAO.

RESULT:
We found that the administration of ALA after cerebral I/R injury reduced cerebral infarction, brain edema, and improved neurologic deficits and cognitive impairment. In parallel, ALA reduced the expressions of APP, BACE1, Aβ and phosphorylated tau in the hippocampus, down-regulated the activation of GSK-3β and microglia, and improved integrity of neuronal synapses.

DISCUSSION:
ALA alleviated the severity of cerebral I/R injury and AD-like pathologies, preserved neuronal integrity, and improved cognitive impairment by down-regulating the activation of GSK-3β and microglia.


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