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Neurosci Lett. 2018 Aug 24;682:39-44. doi: 10.1016/j.neulet.2018.06.008. Epub 2018 Jun 6.

Monosodium glutamate exposure during the neonatal period leads to cognitive deficits in adult Sprague-Dawley rats.

Author information

1
Department of Pathophysiology, Henan Medical College, Zhengzhou 451191, China; Henan Medical Key Laboratory of Cerebrodegenerative Disease, Henan Medical College, Zhengzhou 451191, China. Electronic address: 2016010011@hamc.edu.cn.
2
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, China; Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jie-Fang Avenue, Wuhan 430030, China.
3
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, China; Department of Cardiology, West China Hospital, Sichuan University, 37 Guo Xue Xiang,Chengdu 610041, China.
4
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, China; Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
5
Department of Pathology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
6
Department of Pathology, Wuhan Children's Hospital, Wuhan, 430016, China.
7
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, China.
8
Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, No. 8 Longyuan Road, Nanshan District, Shenzhen 518055, China.
9
Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, No. 8 Longyuan Road, Nanshan District, Shenzhen 518055, China. Electronic address: xifeiyang@szcdc.net.
10
Department of Pathophysiology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, China; Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, China. Electronic address: liugp111@mail.hust.edu.cn.

Abstract

Epidemiological surveys show that 70-80% of patients with Alzheimer's disease (AD) have type 2 diabetes mellitus (T2DM) or show an abnormality of blood glucose levels. Therefore, an increasing number of evidence has suggested that diabetic hyperglycemia is tightly linked with the pathogenesis and progression of AD. In the present study, we replicated T2DM animal model via subcutaneous injection of newborn Sprague-Dawley (SD) rats with monosodium glutamate (MSG) during the neonatal period to investigate the effects and underlying mechanisms of hyperglycemia on cognitive ability. We found that neonatal MSG exposure induced hyperglycemia as well as Alzheimer-like learning and memory deficits with decreased dendritic spine density and hippocampal synaptic-related protein expression and increased phosphorylated tau levels in ∼3-month-old SD rats. Our results suggested that hyperglycemia probably causes cognitive impairment and Alzheimer-like neuropathological changes, which provide the experimental data connecting T2DM and AD.

KEYWORDS:

Alzheimer’s disease; Cognitive deficits; Monosodium glutamate; Plasticity-related proteins; Tau hyperphosphorylation

PMID:
29885453
DOI:
10.1016/j.neulet.2018.06.008
[Indexed for MEDLINE]

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