scholarly journals 5‐HT6R null mutatrion induces synaptic and cognitive defects

Aging Cell ◽  
2021 ◽  
Author(s):  
Zehui Sun ◽  
Bingjie Wang ◽  
Chen Chen ◽  
Chenjian Li ◽  
Yan Zhang
Keyword(s):  
Cognitive Defects

scholarly journals Characterization of a Drosophila Alzheimer's Disease Model: Pharmacological Rescue of Cognitive Defects

PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e20799 ◽  
Author(s):  
Ranjita Chakraborty ◽  
Vidya Vepuri ◽  
Siddhita D. Mhatre ◽  
Brie E. Paddock ◽  
Sean Miller ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Cognitive Defects

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.

scholarly journals Paradoxical Relationship between Mn Superoxide Dismutase Deficiency and Radiation-Induced Cognitive Defects

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49367 ◽  
Author(s):  
Rikki Corniola ◽  
Yani Zou ◽  
David Leu ◽  
John R. Fike ◽  
Ting-Ting Huang
Keyword(s):  
Superoxide Dismutase ◽  
Radiation Induced ◽  
Cognitive Defects
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