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(-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease.
Neuroreport. 2017 Jul 05; 28(10):590-597.N

Abstract

(-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic extract in green tea and it has attracted increasing attention for its multiple bioactive effects. However, the mechanisms by which EGCG exerts its neuroprotective actions in Alzheimer's disease (AD) are presently lacking. In the present study, a sporadic AD transgenic mouse model known as senescence-accelerated mouse prone 8 (SAMP8) was used to investigate whether oral administration of EGCG could improve recognition and memory function through reduction of amyloid β (Aβ) and tau hyperphosphorylation. We also investigated the effects of chronic EGCG treatment on the synaptic dysfunction in the frontal cortex (FC) and the hippocampus (Hip) of AD mice. The results showed that long-term oral consumption of EGCG at a relatively high dose (15 mg/kg) improved memory function in SAMP8 mice in the Y-maze and Morris water maze. The levels of Aβ1-42 and BACE-1 in FC and Hip were significantly reduced by EGCG treatment. EGCG treatment also prevented the hyperphosphorylation of tau and reversed the decreased synaptic protein marker synaptophysin and postsynaptic density protein 95 in FC and Hip of SAMP8 mice. The present study suggests that long-term oral consumption of EGCG ameliorates impairments in spatial learning and memory and rescues the reduction in synaptic proteins observed in an AD mouse model. Thus, EGCG may represent a novel candidate agent for the treatment of neurodegenerative diseases.

Authors+Show Affiliations

Department of Pathophysiology, Institute of Basic Medicine Science, Xi'an Medical University, Xi'an, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28520620

Citation

Guo, Yufang, et al. "(-)-Epigallocatechin-3-gallate Ameliorates Memory Impairment and Rescues the Abnormal Synaptic Protein Levels in the Frontal Cortex and Hippocampus in a Mouse Model of Alzheimer's Disease." Neuroreport, vol. 28, no. 10, 2017, pp. 590-597.
Guo Y, Zhao Y, Nan Y, et al. (-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease. Neuroreport. 2017;28(10):590-597.
Guo, Y., Zhao, Y., Nan, Y., Wang, X., Chen, Y., & Wang, S. (2017). (-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease. Neuroreport, 28(10), 590-597. https://doi.org/10.1097/WNR.0000000000000803
Guo Y, et al. (-)-Epigallocatechin-3-gallate Ameliorates Memory Impairment and Rescues the Abnormal Synaptic Protein Levels in the Frontal Cortex and Hippocampus in a Mouse Model of Alzheimer's Disease. Neuroreport. 2017 Jul 5;28(10):590-597. PubMed PMID: 28520620.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - (-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease. AU - Guo,Yufang, AU - Zhao,Yan, AU - Nan,Ying, AU - Wang,Xiang, AU - Chen,Yulong, AU - Wang,Shuang, PY - 2017/5/19/pubmed PY - 2018/3/23/medline PY - 2017/5/19/entrez SP - 590 EP - 597 JF - Neuroreport JO - Neuroreport VL - 28 IS - 10 N2 - (-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic extract in green tea and it has attracted increasing attention for its multiple bioactive effects. However, the mechanisms by which EGCG exerts its neuroprotective actions in Alzheimer's disease (AD) are presently lacking. In the present study, a sporadic AD transgenic mouse model known as senescence-accelerated mouse prone 8 (SAMP8) was used to investigate whether oral administration of EGCG could improve recognition and memory function through reduction of amyloid β (Aβ) and tau hyperphosphorylation. We also investigated the effects of chronic EGCG treatment on the synaptic dysfunction in the frontal cortex (FC) and the hippocampus (Hip) of AD mice. The results showed that long-term oral consumption of EGCG at a relatively high dose (15 mg/kg) improved memory function in SAMP8 mice in the Y-maze and Morris water maze. The levels of Aβ1-42 and BACE-1 in FC and Hip were significantly reduced by EGCG treatment. EGCG treatment also prevented the hyperphosphorylation of tau and reversed the decreased synaptic protein marker synaptophysin and postsynaptic density protein 95 in FC and Hip of SAMP8 mice. The present study suggests that long-term oral consumption of EGCG ameliorates impairments in spatial learning and memory and rescues the reduction in synaptic proteins observed in an AD mouse model. Thus, EGCG may represent a novel candidate agent for the treatment of neurodegenerative diseases. SN - 1473-558X UR - https://www.unboundmedicine.com/medline/citation/28520620/____Epigallocatechin_3_gallate_ameliorates_memory_impairment_and_rescues_the_abnormal_synaptic_protein_levels_in_the_frontal_cortex_and_hippocampus_in_a_mouse_model_of_Alzheimer's_disease_ L2 - https://doi.org/10.1097/WNR.0000000000000803 DB - PRIME DP - Unbound Medicine ER -