scholarly journals Studies for Improving a Rat Model of Alzheimer’s Disease: Icv Administration of Well-Characterized β-Amyloid 1-42 Oligomers Induce Dysfunction in Spatial Memory

Molecules ◽  
2017 ◽  
Vol 22 (11) ◽  
pp. 2007 ◽  
Author(s):  
Ágnes Kasza ◽  
Botond Penke ◽  
Zsuzsanna Frank ◽  
Zsolt Bozsó ◽  
Viktor Szegedi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Rat Model ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

Effect of Camellia sinensis on Spatial Memory in a Rat Model of Alzheimer’s Disease

2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Tahereh Mahmoodzadeh ◽  
Maryam Haji Khasem Kashani ◽  
Hassan Ramshini ◽  
Alireza Moslem ◽  
Mohammad Mohammad-Zadeh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Camellia Sinensis ◽  
Rat Model ◽  
Model Of Alzheimer’S Disease

scholarly journals Effects of Cyperus rotundus Extract on Spatial Memory Impairment and Neuronal Differentiation in Rat Model of Alzheimer's Disease

2020 ◽  
Vol 9 (1) ◽  
pp. 17
Author(s):  
Ebrahim Esfandiari ◽  
Zeinab Shakerin ◽  
Shahnaz Razavi ◽  
Hojjatallah Alaei ◽  
Mustafa Ghanadian ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Neuronal Differentiation ◽  
Rat Model ◽  
Memory Impairment ◽  
Cyperus Rotundus ◽  
Model Of Alzheimer’S Disease

scholarly journals The Effect of Spironolactone on β-amyloid-Induced Memory Impairment in Male Rats: The Role of Microglial Inhibition

2021 ◽  
Author(s):  
Mohammad Mehdipour ◽  
Masoumeh Emamghoreishi ◽  
Majid Reza Farrokhi ◽  
Elahe Amirinezhadfard ◽  
Mojtaba Keshavarz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Memory Impairment ◽  
Microglial Activation ◽  
Memory Loss ◽  
Inhibitory Avoidance ◽  
Male Rats ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

Purpose: Neuroinflammation was indicated in the pathophysiology of Alzheimer’s disease. Previous reports have also signified that spironolactone has anti-inflammatory effects. Therefore, the aim of this study was to assess the modulatory effects of spironolactone on neuroinflammation and memory loss in a rat model of Alzheimer’s disease. Methods: The β-amyloid protein fragment 25-35 (Aβ) was injected in the dorsal hippocampus (5μg/2.5μl each side) of male Sprague-Dawley rats for four consecutive days to induce memory impairment. Animals have intraperitoneally received spironolactone (10, 25, or 50 mg/kg, N=6/group) or vehicle for 14 days. The passive inhibitory avoidance and the novel recognition tests were used for memory evaluation. Neuroinflammation was assessed by measuring the level of Iba1 protein, a marker of microglial activation, using western immunoblotting. Results: Different doses of spironolactone showed no significant changes in latency times and discriminations ratios in passive inhibitory avoidance and novel recognition tests, respectively, as compared to vehicle. However, spironolactone-treated groups showed significantly lower Iba1 protein levels in comparison to the vehicle-treated group (p<0.01). Conclusion: Spironolactone had a modulatory effect on neuroinflammation through a repressive effect on microglial activation with no valuable effect on memory improvement in a rat model of Alzheimer’s disease. The findings of this study suggest that Ab-induced memory loss may not be directly linked to microglial activation. Spironolactone may be a potential candidate to be examined in other neuroinflammatory disorders.

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