Reduction of Blood Amyloid-β Oligomers in Alzheimer’s Disease Transgenic Mice by c-Abl Kinase Inhibition

2016 ◽  
Vol 54 (3) ◽  
pp. 1193-1205 ◽  
Author(s):  
Lisbell D. Estrada ◽  
David Chamorro ◽  
María José Yañez ◽  
Marcelo Gonzalez ◽  
Nancy Leal ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Kinase Inhibition ◽  
Abl Kinase

O3-01-01: Amyloid-β protofibrils are linked to cognitive impairment in Alzheimer's disease transgenic mice

2008 ◽  
Vol 4 ◽  
pp. T157-T157
Author(s):  
Anna Lord ◽  
Hillevi Englund ◽  
Fredrik Clausen ◽  
Lars Hillered ◽  
Frida Ekholm Pettersson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Transgenic Mice ◽  
Amyloid Β

scholarly journals N,N′-Diacetyl-p-phenylenediamine restores microglial phagocytosis and improves cognitive defects in Alzheimer’s disease transgenic mice

2019 ◽  
Vol 116 (47) ◽  
pp. 23426-23436 ◽  
Author(s):  
Min Hee Park ◽  
Misun Lee ◽  
Geewoo Nam ◽  
Mingeun Kim ◽  
Juhye Kang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Causative Factor ◽  
Central Feature ◽  
Microglial Phagocytosis ◽  
Cognitive Defects

As a central feature of neuroinflammation, microglial dysfunction has been increasingly considered a causative factor of neurodegeneration implicating an intertwined pathology with amyloidogenic proteins. Herein, we report the smallest synthetic molecule (N,N′-diacetyl-p-phenylenediamine [DAPPD]), simply composed of a benzene ring with 2 acetamide groups at the para position, known to date as a chemical reagent that is able to promote the phagocytic aptitude of microglia and subsequently ameliorate cognitive defects. Based on our mechanistic investigations in vitro and in vivo, 1) the capability of DAPPD to restore microglial phagocytosis is responsible for diminishing the accumulation of amyloid-β (Aβ) species and significantly improving cognitive function in the brains of 2 types of Alzheimer’s disease (AD) transgenic mice, and 2) the rectification of microglial function by DAPPD is a result of its ability to suppress the expression of NLRP3 inflammasome-associated proteins through its impact on the NF-κB pathway. Overall, our in vitro and in vivo investigations on efficacies and molecular-level mechanisms demonstrate the ability of DAPPD to regulate microglial function, suppress neuroinflammation, foster cerebral Aβ clearance, and attenuate cognitive deficits in AD transgenic mouse models. Discovery of such antineuroinflammatory compounds signifies the potential in discovering effective therapeutic molecules against AD-associated neurodegeneration.

Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice

1997 ◽  
Vol 3 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Martin Citron ◽  
David Westaway ◽  
Weiming Xia ◽  
George Carlson ◽  
Thekla Diehl ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Transfected Cells ◽  
Β Protein

scholarly journals Cerebellar Amyloid-β Plaques: Disturbed Cortical Circuitry in AβPP/PS1 Transgenic Mice as a Model of Familial Alzheimer's Disease

2012 ◽  
Vol 31 (2) ◽  
pp. 285-300 ◽  
Author(s):  
Selene Lomoio ◽  
Irene López-González ◽  
Ester Aso ◽  
Margarita Carmona ◽  
Benjamín Torrejón-Escribano ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
Familial Alzheimer’S Disease ◽  
Cortical Circuitry ◽  
Familial Alzheimer's Disease

scholarly journals Blocking the apolipoprotein E/Amyloid β interaction in triple transgenic mice ameliorates Alzheimer's disease related amyloid β and tau pathology

2013 ◽  
Vol 128 (4) ◽  
pp. 577-591 ◽  
Author(s):  
Shan Liu ◽  
Ariel Breitbart ◽  
Yanjie Sun ◽  
Pankaj D. Mehta ◽  
Allal Boutajangout ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Apolipoprotein E ◽  
Amyloid Β ◽  
Tau Pathology
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