scholarly journals Cornel iridoid glycoside ameliorates cognitive deficits in APP/PS1/tau triple transgenic mice by attenuating amyloid‐beta, tau, and neurotrophic dysfunction

2020 ◽  
Vol 16 (S9) ◽  
Author(s):  
Cuicui Yang ◽  
Lan Zhang
Keyword(s):  
Transgenic Mice ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Iridoid Glycoside ◽  
Cornel Iridoid Glycoside

P4-334: Combination of memantine and donepezil reverses cognitive deficits in transgenic mice with both amyloid-beta plaques and neurofibrillary tangles

2009 ◽  
Vol 5 (4S_Part_17) ◽  
pp. e29-e29 ◽  
Author(s):  
Frank M. LaFerla ◽  
Hilda Martinez-Coria ◽  
Kim N. Green ◽  
Pradeep K. Banerjee
Keyword(s):  
Transgenic Mice ◽  
Amyloid Beta ◽  
Cognitive Deficits ◽  
Neurofibrillary Tangles

scholarly journals Cornel Iridoid Glycoside Protects Against STAT1-Dependent Synapse and Memory Deficits by Increasing N-Methyl-D-aspartate Receptor Expression in a Tau Transgenic Mice

2021 ◽  
Vol 13 ◽  
Author(s):  
Denglei Ma ◽  
Rui Huang ◽  
Kaiwen Guo ◽  
Zirun Zhao ◽  
Weipeng Wei ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Chinese Herb ◽  
Microscopy Study ◽  
Iridoid Glycoside ◽  
Receptor Expression ◽  
Janus Kinase ◽  
Synaptic Dysfunction ◽  
Intragastric Administration ◽  
Tau Pathology ◽  
Cornel Iridoid Glycoside

P301S transgenic mice are an animal model of tauopathy and Alzheimer’s disease (AD), exhibiting tau pathology and synaptic dysfunction. Cornel iridoid glycoside (CIG) is an active ingredient extracted from Cornus officinalis, a traditional Chinese herb. In the present study, the purpose was to investigate the effects and mechanisms of CIG on tau pathology and synaptic dysfunction using P301S transgenic mice. The results showed that intragastric administration of CIG for 3.5 months improved cognitive impairments and the survival rate of P301S mice. Electrophysiological recordings and transmission electron microscopy study showed that CIG improved synaptic plasticity and increased the ultrastructure and number of synapse. Moreover, CIG increased the expression levels of N-methyl-D-aspartate receptors (NMDAR) subunits GluN1, GluN2A, and GluN2B, and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) subunit GluA1. We inferred that the major mechanism of CIG involving in the regulation of synaptic dysfunctions was inhibiting the activation of Janus kinase-2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) signaling pathway and alleviating STAT1-induced suppression of NMDAR expressions. Based on our findings, we thought CIG might be a promising candidate for the therapy of tauopathy such as AD.

Mitochondrial failure precedes amyloid beta plaques deposition in APP transgenic mice

2005 ◽  
Vol 38 (05) ◽  
Author(s):  
A Eckert ◽  
I Scherping ◽  
A Bonert ◽  
S Hauptmann ◽  
F Müller-Spahn ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Amyloid Beta

MiR-335-5p Inhibits β-Amyloid (Aβ) Accumulation to Attenuate Cognitive Deficits Through Targeting c-jun-N-terminal Kinase 3 in Alzheimer’s Disease

2020 ◽  
Vol 17 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Dan Wang ◽  
Zhifu Fei ◽  
Song Luo ◽  
Hai Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Western Blot ◽  
Mrna Expression ◽  
Cognitive Deficits ◽  
Protein Levels ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
The Relationship

Objectives: Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs (miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progression of AD is still not clearly clarified. Methods: The protein and mRNA levels were measured by western blot and RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual-luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice were used as an in vivo AD model. Morris water maze test was performed to assess the effect of miR- 335-5p on the cognitive deficits in APP/PS1 transgenic mice. Results: The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated, and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients. The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, the dual Luciferase assay verified the relationship between miR-335- 5p and JNK3. Overexpression of miR-335-5p significantly decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved the cognitive abilities of APP/PS1 mice. Conclusion: The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, may be a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment.

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