scholarly journals Epigallocatechin-3-Gallate Provides Protection Against Alzheimer’s Disease-Induced Learning and Memory Impairments in Rats

2021 ◽  
Vol Volume 15 ◽  
pp. 2013-2024
Author(s):  
Shanji Nan ◽  
Peng Wang ◽  
Yizhi Zhang ◽  
Jia Fan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Memory Impairments

scholarly journals Early Hippocampal Sharp-Wave Ripple Deficits Predict Later Learning and Memory Impairments in an Alzheimer’s Disease Mouse Model

Cell Reports ◽  
2019 ◽  
Vol 29 (8) ◽  
pp. 2123-2133.e4 ◽  
Author(s):  
Emily A. Jones ◽  
Anna K. Gillespie ◽  
Seo Yeon Yoon ◽  
Loren M. Frank ◽  
Yadong Huang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Memory Impairments ◽  
Sharp Wave

scholarly journals Therapeutic Effect of Yi-Chi-Tsung-Ming-Tang on Amyloidβ1−40-Induced Alzheimer's Disease-Like Phenotype via an Increase of Acetylcholine and Decrease of Amyloidβ

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Chung-Hsin Yeh ◽  
Ming-Tsuen Hsieh ◽  
Chi-Mei Hsueh ◽  
Chi-Rei Wu ◽  
Yi-Chun Huang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oral Administration ◽  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Senile Dementia ◽  
High Dose ◽  
Memory Impairments ◽  
Beneficial Role ◽  
Amyloid Accumulation

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by amyloid accumulation, neuronal death, and cognitive impairments. Yi-Chi-Tsung-Ming-Tang (YCTMT) is a traditional Chinese medicine and has never been used to enhance cognitive function and treat neurodegenerative disorders such as senile dementia. Whether YCTMT has a beneficial role in improving learning and memory in AD patients remains unclear. The present study showed that oral administration of YCTMT ameliorated amyloid-β- (Aβ1−40) injection-induced learning and memory impairments in rats, examined using passive avoidance and Morris water-maze tests. Immunostaining and Western Blot results showed that continuous Aβ1−40infusion caused amyloid accumulation and decreased acetylcholine level in hippocampus. Oral administration of medium and high dose of YCTMT 7 days after the Aβ1−40infusion decreased amyloid accumulation area and reversed acetylcholine decline in the Aβ1−40-injected hippocampus, suggesting that YCTMT might inhibit Aβplague accumulation and rescue reduced acetylcholine expression. This study has provided evidence on the beneficial role of YCTMT in ameliorating amyloid-induced AD-like symptom, indicating that YCTMT may offer an alternative strategy for treating AD.

P2-450: Hemizygous deletion of synaptojanin1 ameliorates learning and memory impairments in a mouse model of Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. e8-e8
Author(s):  
Laura Beth J. McIntire ◽  
Diego Berman ◽  
Jennifer Myaeng ◽  
Agniezka Staniszewski ◽  
Ottavio Arancio ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Memory Impairments ◽  
Hemizygous Deletion ◽  
Model Of Alzheimer’S Disease

scholarly journals AβDamages Learning and Memory in Alzheimer’s Disease Rats with Kidney-Yang Deficiency

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Dongmei Qi ◽  
Yongfa Qiao ◽  
Xin Zhang ◽  
Huijuan Yu ◽  
Bin Cheng ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Receptor Internalization ◽  
Spatial Learning And Memory ◽  
Memory Impairments ◽  
Kidney Yang Deficiency ◽  
Kidney Essence

Previous studies demonstrated that Alzheimer’s disease was considered as the consequence produced by deficiency of Kidney essence. However, the mechanism underlying the symptoms also remains elusive. Here we report that spatial learning and memory, escape, and swimming capacities were damaged significantly in Kidney-yang deficiency rats. Indeed, both hippocampal Aβ40and 42 increases in Kidney-yang deficiency contribute to the learning and memory impairments. Specifically, damage of synaptic plasticity is involved in the learning and memory impairment of Kidney-yang deficiency rats. We determined that the learning and memory damage in Kidney-yang deficiency due to synaptic plasticity impairment and increases of Aβ40and 42 was not caused via NMDA receptor internalization induced by Aβincrease.β-Adrenergic receptor agonist can rescue the impaired long-term potential (LTP) in Kidney-yang rats. Taken together, our results suggest that spatial learning and memory inhibited in Kidney-yang deficiency might be induced by Aβincrease and the decrease ofβ2receptor function in glia.

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