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(-)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice.
Mol Neurobiol. 2014 Jun; 49(3):1350-63.MN

Abstract

Alzheimer's disease (AD) is pathologically characterized by deposition of β-amyloid (Aβ) peptides, which closely correlates with the balance of nerve growth factor (NGF)-related TrkA/p75NTR signaling. (-)-Epigallocatechin-3-gallate (EGCG) is used for prevention and treatment of many neurodegenerative diseases, including AD. However, whether the neuroprotective effects of EGCG treatment were via modulating the balance of TrkA/p75NTR signaling was still unknown. In this study, we found that EGCG treatment (2 mg·kg(-1)·day(-1)) dramatically ameliorated the cognitive impairments, reduced the overexpressions of Aβ(1-40) and amyloid precursor protein (APP), and inhibited the neuronal apoptosis in the APP/PS1 mice. Interestingly, the EGCG treatment enhanced the relative expression level of NGF by increasing the NGF/proNGF ratio in the APP/PS1 mice. Moreover, after EGCG treatment, TrkA signaling was activated by increasing the phosphorylation of TrkA following the increased phosphorylation of c-Raf, ERK1/2, and cAMP response element-binding protein (CREB), simultaneously the p75NTR signaling was significantly inhibited by decreasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression, so that the Aβ deposits and neuronal apoptosis in the hippocampus were inhibited.

Authors+Show Affiliations

Department of Pharmacology, School of Pharmaceutical Sciences, China Medical University, No.92 Bei'er Road, Heping District, Shenyang, 110001, Liaoning Province, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24356899

Citation

Liu, Mingyan, et al. "(-)-Epigallocatechin-3-gallate Ameliorates Learning and Memory Deficits By Adjusting the Balance of TrkA/p75NTR Signaling in APP/PS1 Transgenic Mice." Molecular Neurobiology, vol. 49, no. 3, 2014, pp. 1350-63.
Liu M, Chen F, Sha L, et al. (-)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice. Mol Neurobiol. 2014;49(3):1350-63.
Liu, M., Chen, F., Sha, L., Wang, S., Tao, L., Yao, L., He, M., Yao, Z., Liu, H., Zhu, Z., Zhang, Z., Zheng, Z., Sha, X., & Wei, M. (2014). (-)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice. Molecular Neurobiology, 49(3), 1350-63. https://doi.org/10.1007/s12035-013-8608-2
Liu M, et al. (-)-Epigallocatechin-3-gallate Ameliorates Learning and Memory Deficits By Adjusting the Balance of TrkA/p75NTR Signaling in APP/PS1 Transgenic Mice. Mol Neurobiol. 2014;49(3):1350-63. PubMed PMID: 24356899.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - (-)-Epigallocatechin-3-gallate ameliorates learning and memory deficits by adjusting the balance of TrkA/p75NTR signaling in APP/PS1 transgenic mice. AU - Liu,Mingyan, AU - Chen,Fujun, AU - Sha,Lei, AU - Wang,Shuang, AU - Tao,Lin, AU - Yao,Lutian, AU - He,Miao, AU - Yao,Zhimin, AU - Liu,Hang, AU - Zhu,Zheng, AU - Zhang,Zhenjie, AU - Zheng,Zhihong, AU - Sha,Xianzheng, AU - Wei,Minjie, Y1 - 2013/12/20/ PY - 2013/07/29/received PY - 2013/12/08/accepted PY - 2013/12/21/entrez PY - 2013/12/21/pubmed PY - 2015/1/27/medline SP - 1350 EP - 63 JF - Molecular neurobiology JO - Mol. Neurobiol. VL - 49 IS - 3 N2 - Alzheimer's disease (AD) is pathologically characterized by deposition of β-amyloid (Aβ) peptides, which closely correlates with the balance of nerve growth factor (NGF)-related TrkA/p75NTR signaling. (-)-Epigallocatechin-3-gallate (EGCG) is used for prevention and treatment of many neurodegenerative diseases, including AD. However, whether the neuroprotective effects of EGCG treatment were via modulating the balance of TrkA/p75NTR signaling was still unknown. In this study, we found that EGCG treatment (2 mg·kg(-1)·day(-1)) dramatically ameliorated the cognitive impairments, reduced the overexpressions of Aβ(1-40) and amyloid precursor protein (APP), and inhibited the neuronal apoptosis in the APP/PS1 mice. Interestingly, the EGCG treatment enhanced the relative expression level of NGF by increasing the NGF/proNGF ratio in the APP/PS1 mice. Moreover, after EGCG treatment, TrkA signaling was activated by increasing the phosphorylation of TrkA following the increased phosphorylation of c-Raf, ERK1/2, and cAMP response element-binding protein (CREB), simultaneously the p75NTR signaling was significantly inhibited by decreasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression, so that the Aβ deposits and neuronal apoptosis in the hippocampus were inhibited. SN - 1559-1182 UR - https://www.unboundmedicine.com/medline/citation/24356899/____Epigallocatechin_3_gallate_ameliorates_learning_and_memory_deficits_by_adjusting_the_balance_of_TrkA/p75NTR_signaling_in_APP/PS1_transgenic_mice_ L2 - https://dx.doi.org/10.1007/s12035-013-8608-2 DB - PRIME DP - Unbound Medicine ER -