scholarly journals Tripchlorolide improves cognitive deficits by reducing amyloid β and upregulating synapse-related proteins in a transgenic model of Alzheimer's Disease

2015 ◽  
Vol 133 (1) ◽  
pp. 38-52 ◽  
Author(s):  
Yuqi Zeng ◽  
Jian Zhang ◽  
Yuangui Zhu ◽  
Jing Zhang ◽  
Hui Shen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Amyloid Β ◽  
Transgenic Model ◽  
Model Of Alzheimer’S Disease ◽  
Related Proteins

scholarly journals Carboxy-Terminus Tau Protein Hyperphosphorylation is Associated with Extracellular Deposits of Amyloid-β Fibrillary in a Triple-Transgenic Model of Alzheimer’s Disease

2017 ◽  
Vol 05 (03) ◽  
Author(s):  
Miguel Angel Ontiveros Torres ◽  
Leonel Castellanos Aguilar ◽  
Jonathan Lennel Gutierrez Murcia ◽  
Nayeli Martinez Zuniga ◽  
Paola Flores Rodriguez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tau Protein ◽  
Amyloid Β ◽  
Carboxy Terminus ◽  
Transgenic Model ◽  
Model Of Alzheimer’S Disease

scholarly journals Pharmacological activation of the nuclear receptor REV-ERB reverses cognitive deficits and reduces amyloid-β burden in a mouse model of Alzheimer’s disease

PLoS ONE ◽  
2019 ◽  
Vol 14 (4) ◽  
pp. e0215004 ◽  
Author(s):  
Deborah A. Roby ◽  
Fernanda Ruiz ◽  
Bailey A. Kermath ◽  
Jaymie R. Voorhees ◽  
Michael Niehoff ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Nuclear Receptor ◽  
Cognitive Deficits ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease

scholarly journals Naphthalene monoimide derivative ameliorates amyloid burden and cognitive decline in a transgenic mouse model of Alzheimer’s disease

2020 ◽  
Author(s):  
Sourav Samanta ◽  
Kolla Rajasekhar ◽  
Madhu Ramesh ◽  
N. Arul Murugan ◽  
Shadab Alam ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficits ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Salt Bridges ◽  
Amyloid Burden ◽  
Amyloid Toxicity ◽  
Model Of Alzheimer’S Disease

ABSTRACTAlzheimer’s disease (AD) is a major neurodegenerative disorder and the leading cause of dementia worldwide. Predominantly, misfolding and aggregation of amyloid-β (Aβ) peptides associated with multifaceted toxicity is the neuropathological hallmark of AD pathogenesis and thus, primary therapeutic target to ameliorate neuronal toxicity and cognitive deficits. Herein, we report the design, synthesis and evaluation of small molecule inhibitors with naphthalene monoimide scaffold to ameliorate in vitro and in vivo amyloid induced neurotoxicity. The detailed studies established TGR63 as the lead candidate to rescue neuronal cells from amyloid toxicity. The in silico studies showed disruption of salt bridges and intermolecular hydrogen bonding interactions within Aβ42 fibrils by the interaction of TGR63, causing destabilization of Aβ42 assembly. Remarkably, TGR63 treatment showed a significant reduction in cortical and hippocampal amyloid burden in the progressive stages of APP/PS1 AD mice brain. Various behavioral tests demonstrated rescued cognitive deficits. The excellent biocompatibility, BBB permeability and therapeutic efficacy to reduce amyloid burden make TGR63 a promising candidate for the treatment of AD.

scholarly journals Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-β Levels in a Mouse Model of Alzheimer's Disease

PLoS ONE ◽  
2010 ◽  
Vol 5 (4) ◽  
pp. e9979 ◽  
Author(s):  
Patricia Spilman ◽  
Natalia Podlutskaya ◽  
Matthew J. Hart ◽  
Jayanta Debnath ◽  
Olivia Gorostiza ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Deficits ◽  
Amyloid Β ◽  
Model Of Alzheimer’S Disease
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