scholarly journals FTIR imaging of the molecular burden around Aβ deposits in an early-stage 3-Tg-APP-PSP1-TAU mouse model of Alzheimer's disease

The Analyst ◽  
2017 ◽  
Vol 142 (1) ◽  
pp. 156-168 ◽  
Author(s):  
Artur Dawid Surowka ◽  
Michael Pilling ◽  
Alex Henderson ◽  
Herve Boutin ◽  
Lidan Christie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Spatial Resolution ◽  
Mouse Brain ◽  
High Spatial Resolution ◽  
Early Stage ◽  
Ftir Imaging ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model

High spatial resolution FTIR imaging of early-stage 3-Tg-APP-PSP1-TAU mouse brain identifies molecular burden around Aβ deposits.

scholarly journals P2-067: EFFECTS OF THE NEUROGENIC MOLECULE NSI-189 ON INDICES OF COGNITION IN AN APP/TAU MOUSE MODEL OF ALZHEIMER'S DISEASE

2019 ◽  
Vol 15 ◽  
pp. P596-P596
Author(s):  
Corinne G. Jolivalt ◽  
Alexandra Marquez ◽  
Lisa Guernsey ◽  
David M. Quach ◽  
Karl K. Johe
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model

scholarly journals Inhibition of 2-Arachidonoylglycerol Metabolism Alleviates Neuropathology and Improves Cognitive Function in a Tau Mouse Model of Alzheimer’s Disease

2021 ◽  
Author(s):  
Jack Hashem ◽  
Mei Hu ◽  
Jian Zhang ◽  
Fei Gao ◽  
Chu Chen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Therapeutic Target ◽  
The United States ◽  
Synaptic Proteins ◽  
Spatial Learning And Memory ◽  
Memory Retention ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model

Abstract Alzheimer's disease (AD) is the most common cause of dementia, which affects more than 5 million individuals in the United States. Unfortunately, no effective therapies are currently available to prevent development of AD or to halt progression of the disease. It has been proposed that monoacylglycerol lipase (MAGL), the key enzyme degrading the endocannabinoid 2-arachidonoylglycerol (2-AG) in the brain, is a therapeutic target for AD based on the studies using the APP transgenic models of AD. While inhibition of 2-AG metabolism mitigates b-amyloid (Aβ) neuropathology, it is still not clear whether inactivation of MAGL alleviates tauopathies as accumulation and deposition of intracellular hyperphosphorylated tau protein are the neuropathological hallmark of AD. Here we show that JZL184, a potent MAGL inhibitor, significantly reduced proinflammatory cytokines, astrogliosis, phosphorylated tau, and GSK3b in P301S/PS19 mice, a tau mouse model of AD. Importantly, Tau transgenic mice treated with JZL184 displayed improvements in spatial learning and memory retention. In addition, inactivation of MAGL ameliorates deteriorations in expression of synaptic proteins in P301S/PS19 mice. Our results provide further evidence that MAGL is a promising therapeutic target for AD.

Multi-target PET evaluation in APP/PS1/tau mouse model of Alzheimer’s disease

2020 ◽  
Vol 728 ◽  
pp. 134938 ◽  
Author(s):  
Yu Liu ◽  
Yuping Xu ◽  
Mingzhu Li ◽  
Donghui Pan ◽  
Yaoqi Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model

scholarly journals Haloperidol inactivates AMPK and reduces tau phosphorylation in a tau mouse model of Alzheimer's disease

2016 ◽  
Vol 2 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Jeremy Koppel ◽  
Heidy Jimenez ◽  
Leslie Adrien ◽  
Blaine S. Greenwald ◽  
Philippe Marambaud ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Tau Phosphorylation ◽  
Model Of Alzheimer’S Disease ◽  
Tau Mouse Model
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