Faculty Opinions recommendation of Activation of the amyloid cascade in apolipoprotein E4 transgenic mice induces lysosomal activation and neurodegeneration resulting in marked cognitive deficits.

2008 ◽  
Author(s):  
Jean-Charles Lambert
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Apolipoprotein E4 ◽  
Amyloid Cascade

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.

Aβ levels in serum, CSF and brain, and cognitive deficits in APP + PS1 transgenic mice

Neuroreport ◽  
2003 ◽  
Vol 14 (1) ◽  
pp. 163-166 ◽  
Author(s):  
Li Liu ◽  
Tero Tapiola ◽  
Sanna-Kaisa Herukka ◽  
Matti Heikkilä ◽  
Heikki Tanila
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits

The beneficial effects of dietary grape supplementation on improving cognitive deficits in APP/PS1 double transgenic mice

2018 ◽  
Vol 49 ◽  
pp. 224-234 ◽  
Author(s):  
Kangliang Sheng ◽  
Shanshan Shui ◽  
Ling Yan ◽  
Junjie Yu ◽  
Guang Hao ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Beneficial Effects ◽  
Double Transgenic Mice

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
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