Soluble Aβ levels correlate with cognitive deficits in the 12-month-old APPswe/PS1dE9 mouse model of Alzheimer's disease

2011 ◽  
Vol 222 (2) ◽  
pp. 342-350 ◽  
Author(s):  
Wei Zhang ◽  
Jian Hao ◽  
Rui Liu ◽  
Zhuo Zhang ◽  
Gesheng Lei ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Deficits ◽  
Model Of Alzheimer’S Disease

P1-033: Cognitive deficits and plaque deposition in a gene-targeted mouse model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_6) ◽  
pp. P181-P181
Author(s):  
John Ciallella ◽  
Heather Hain ◽  
Bryan Strenkowski ◽  
Michelle Hogga ◽  
Stacey Galvin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Deficits ◽  
Plaque Deposition ◽  
Model Of Alzheimer’S Disease

scholarly journals Oral administration of methysticin improves cognitive deficits in a mouse model of Alzheimer's disease

Redox Biology ◽  
2017 ◽  
Vol 12 ◽  
pp. 843-853 ◽  
Author(s):  
Athanassios Fragoulis ◽  
Stephanie Siegl ◽  
Markus Fendt ◽  
Sandra Jansen ◽  
Ulf Soppa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Oral Administration ◽  
Cognitive Deficits ◽  
Model Of Alzheimer’S Disease

scholarly journals Protective effects of edaravone on white matter pathology in a novel mouse model of Alzheimer’s disease with chronic cerebral hypoperfusion

2020 ◽  
pp. 0271678X2096892
Author(s):  
Tian Feng ◽  
Toru Yamashita ◽  
Ryo Sasaki ◽  
Koh Tadokoro ◽  
Namiko Matsumoto ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Mouse Model ◽  
Cognitive Deficits ◽  
Cerebral Hypoperfusion ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Model Of Alzheimer’S Disease ◽  
Promising Therapeutic Approach

White matter lesions (WMLs) caused by cerebral chronic hypoperfusion (CCH) may contribute to the pathophysiology of Alzheimer’s disease (AD). However, the underlying mechanisms and therapeutic approaches have yet to be totally identified. In the present study, we investigated a potential therapeutic effect of the free radical scavenger edaravone (EDA) on WMLs in our previously reported novel mouse model of AD (APP23) plus CCH with motor and cognitive deficits. Relative to AD with CCH mice at 12 months (M) of age, EDA strongly improved CCH-induced WMLs in the corpus callosum of APP23 mice at 12 M by improving the disruption of white matter integrity, enhancing the proliferation of oligodendrocyte progenitor cells, attenuating endothelium/astrocyte unit dysfunction, and reducing neuroinflammation and oxidative stress. The present study demonstrates that the long-term administration of EDA may provide a promising therapeutic approach for WMLs in AD plus CCH disease with cognitive deficits.

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