Chronic cerebral hypoperfusion in a mouse model of Alzheimer's disease: An additional contributing factor of cognitive impairment

2011 ◽  
Vol 489 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Jin Soo Lee ◽  
Doo Soon Im ◽  
Young-Sil An ◽  
Ji Man Hong ◽  
Byoung Joo Gwag ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Model Of Alzheimer’S Disease

β-Lapachone attenuates cognitive impairment and neuroinflammation in beta-amyloid induced mouse model of Alzheimer's disease

2020 ◽  
Vol 81 ◽  
pp. 106300 ◽  
Author(s):  
Narmin Mokarizadeh ◽  
Pouran Karimi ◽  
Marjan Erfani ◽  
Saeed Sadigh-Eteghad ◽  
Nazila Fathi Maroufi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Beta Amyloid ◽  
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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