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209 results on '"Qi, Jin-shun"'

14. (D-Ser2) oxyntomodulin recovers hippocampal synaptic structure and theta rhythm in Alzheimer’s disease transgenic mice

Author

Qi, Jin-Shun, primary, Wang, Zhao-Jun, primary, Yang, Guang-Zhao, additional, Gao, Qi-Chao, additional, Li, Wei-Ran, additional, Cai, Hong-Yan, additional, Zhao, Hui-Min, additional, Wang, Jian-Ji, additional, Zhao, Xin-Rui, additional, Wang, Jia-Xin, additional, Wu, Mei-Na, additional, Zhang, Jun, additional, and Hölscher, Christian, additional

Published
2022
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18. DAla2-GIP-GLU-PAL Protects Against Cognitive Deficits and Pathology in APP/PS1 Mice by Inhibiting Neuroinflammation and Upregulating cAMP/PKA/CREB Signaling Pathways

Author

Yuan, Li, primary, Zhang, Jun, additional, Guo, Jun-Hong, additional, Holscher, Christian, additional, Yang, Jun-Ting, additional, Wu, Mei-Na, additional, Wang, Zhao-Jun, additional, Cai, Hong-Yan, additional, Han, Ling-Na, additional, Shi, Hui, additional, Han, Yu-Fei, additional, and Qi, Jin-Shun, additional

Published
2021
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36. A novel antibody targeting sequence 31-35 in amyloid β protein attenuates Alzheimer's disease-related neuronal damage.

Author

Cheng, Li, Zhang, Jun, Li, Xin‐Yi, Yuan, Li, Pan, Yan‐Fang, Chen, Xiao‐Rong, Gao, Tian‐Ming, Qiao, Jian‐Tian, and Qi, Jin‐Shun

Abstract

ABSTRACT Amyloid β protein (Aβ) plays a critical role in pathogenesis of Alzheimer's disease (AD). Our previous studies indicated that the sequence 31-35 in Aβ molecule is an effective active center responsible for Aβ neurotoxicity in vivo and in vitro. In the present study, we prepared a novel antibody specifically targeting the sequence 31-35 of amyloid β protein, and investigated the neuroprotection of the anti-Aβ31-35 antibody against Aβ1-42-induced impairments in neuronal viability, spatial memory, and hippocampal synaptic plasticity in rats. The results showed that the anti-Aβ31-35 antibody almost equally bound to both Aβ31-35 and Aβ1-42, and pretreatment with the antibody dose-dependently prevented Aβ1-42-induced cytotoxicity on cultured primary cortical neurons. In behavioral study, intracerebroventricular (i.c.v.) injection of anti-Aβ31-35 antibody efficiently attenuated Aβ1-42-induced impairments in spatial learning and memory of rats. In vivo electrophysiological experiments further indicated that Aβ1-42-induced suppression of hippocampal synaptic plasticity was effectively reversed by the antibody. These results demonstrated that the sequence 31-35 of Aβ may be a new therapeutic target, and the anti-Aβ31-35 antibody could be a novel immunotheraputic approach for the treatment of AD. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Published
2017
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43. Desipramine improves depression-like behavior and working memory by up-regulating p-CREB in Alzheimer's disease associated mice.

Author

Wang, Dan-Dan, Li, Jia, Yu, Li-Peng, Wu, Mei-Na, Sun, Li-Na, and Qi, Jin-Shun

Subjects
ALZHEIMER'S disease, AMYLOID beta-protein, AMYLOID plaque, MENTAL depression, COGNITION disorders
Abstract

Aggregation of amyloid protein (A and progressive loss of memory are the main characteristics of Alzheimer's disease (AD). It is noteworthy that approximately 40% of AD patients have depressive symptom. The close correlation between cognitive deficits and mental depression suggests a possibility that antidepression treatment might be beneficial to cognitive improvement in AD. The present study, by using tail-suspension test (TST), forced swimming, alternative electro-stimulus Y maze test and immunohistochemistry, examined the neuroprotective effects of desipramine, a newer generation tricyclic antidepressants (TCA), and investigated its possible molecular mechanism. The results showed that: (1) intra-hippocampal injection of A induced depression-like behavior and associative learning deficits in mice, with an increased mean immobility time in tail-suspension and forced swimming test and an increased mean error times in Y maze test; (2) after treatment with desipramine (10mg/kg, i.p.), the average immobility time significantly decreased, from s in A group to s in A plus desipramine group () in TST and from s to s ( or 9, ) in forced swimming test, respectively;the mean error times of mice in Y maze test also significantly decreased, from in A group to in A plus desipramine group (, ); (3) desipramine administration significantly prevented against A-induced down-regulation of phosphorylated cAMP response element binding protein (p-CREB) in the hippocampus. These results indicate that A could concurrently mimic the depression-like behavior and working memory disorder in mice, while desipramine could effectively reverse both the deficits induced by A. The neuroprotection of desipramine may be involved in the up-regulation of p-CREB level in the hippocampus of mice. [ABSTRACT FROM AUTHOR]

Published
2016
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50. Colivelin ameliorates amyloid β peptide-induced impairments in spatial memory, synaptic plasticity, and calcium homeostasis in rats.

Author

Wu, Mei‐Na, Zhou, Li‐Wei, Wang, Zhao‐Jun, Han, Wei‐Na, Zhang, Jun, Liu, Xiao‐Jie, Tong, Jia‐Qing, and Qi, Jin‐Shun

Abstract

ABSTRACT Amyloid β peptide (Aβ) has been thought to be neurotoxic and responsible for the impairment of learning and memory in Alzheimer's disease (AD). Humanin (HN), a 24 amino acid polypeptide first identified from the unaffected occipital lobe of an AD patient, is believed to be neuroprotective against the AD-related neurotoxicity. In this study, we investigated the neuroprotective effects of Colivelin (CLN), a novel HN derivative, against Aβ by using behavioral test, in vivo electrophysiological recording, and intracellular calcium imaging. Our results showed that intrahippocampal injection of CLN (0.2 nmol) effectively prevented Aβ25-35 (4 nmol)-induced deficits in spatial learning and memory of rats in Morris water maze test; the suppression of in vivo hippocampal long term potentiation (LTP) by Aβ25-35 was nearly completely prevented by CLN; in addition, CLN pretreatment also effectively inhibited Aβ25-35-induced calcium overload in primary cultured hippocampal neurons. These results indicate that CLN has significant neuroprotective properties against Aβ, and CLN may holds great promise for the treatment and prevention of AD. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Published
2015
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