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.

Subtle learning and memory impairment in an idiopathic rat model of Alzheimer's disease utilizing cholinergic depletions and β-amyloid

2016 ◽  
Vol 1646 ◽  
pp. 12-24 ◽  
Author(s):  
S.H. Deibel ◽  
N. Weishaupt ◽  
A.M. Regis ◽  
N.S. Hong ◽  
R.J. Keeley ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Rat Model ◽  
Memory Impairment ◽  
Model Of Alzheimer’S Disease ◽  
Β Amyloid

scholarly journals Noncanonical function of an autophagy protein prevents spontaneous Alzheimer’s disease

2020 ◽  
Vol 6 (33) ◽  
pp. eabb9036
Author(s):  
Bradlee L. Heckmann ◽  
Brett J. W. Teubner ◽  
Emilio Boada-Romero ◽  
Bart Tummers ◽  
Clifford Guy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Disease ◽  
Memory Impairment ◽  
Memory Loss ◽  
Tau Hyperphosphorylation ◽  
Primary Microglia ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
Old Mice

Noncanonical functions of autophagy proteins have been implicated in neurodegenerative conditions, including Alzheimer’s disease (AD). The WD domain of the autophagy protein Atg16L is dispensable for canonical autophagy but required for its noncanonical functions. Two-year-old mice lacking this domain presented with robust β-amyloid (Aβ) pathology, tau hyperphosphorylation, reactive microgliosis, pervasive neurodegeneration, and severe behavioral and memory deficiencies, consistent with human disease. Mechanistically, we found this WD domain was required for the recycling of Aβ receptors in primary microglia. Pharmacologic suppression of neuroinflammation reversed established memory impairment and markers of disease pathology in this novel AD model. Therefore, loss of the Atg16L WD domain drives spontaneous AD in mice, and inhibition of neuroinflammation is a potential therapeutic approach for treating neurodegeneration and memory loss. A decline in expression of ATG16L in the brains of human patients with AD suggests the possibility that a similar mechanism may contribute in human 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

Methanolic Extract of Piper nigrum Fruits Improves Memory Impairment by Decreasing Brain Oxidative Stress in Amyloid Beta(1–42) Rat Model of Alzheimer’s Disease

2014 ◽  
Vol 34 (3) ◽  
pp. 437-449 ◽  
Author(s):  
Lucian Hritcu ◽  
Jaurès A. Noumedem ◽  
Oana Cioanca ◽  
Monica Hancianu ◽  
Victor Kuete ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Rat Model ◽  
Memory Impairment ◽  
Methanolic Extract ◽  
Piper Nigrum ◽  
Model Of Alzheimer’S Disease ◽  
Brain Oxidative Stress

P4-042: Memory impairment in the Tg6590 transgenic rat model of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_15) ◽  
pp. P443-P443
Author(s):  
Eirikur Benedikz ◽  
Therese M. Pham ◽  
Ewa Kloskowska ◽  
Lars O. Pedersen ◽  
Jan T. Pedersen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Memory Impairment ◽  
Transgenic Rat ◽  
Model Of Alzheimer’S Disease ◽  
Transgenic Rat Model

Intranasal deferoxamine affects memory loss, oxidation, and the insulin pathway in the streptozotocin rat model of Alzheimer's disease

2017 ◽  
Vol 380 ◽  
pp. 164-171 ◽  
Author(s):  
J.M. Fine ◽  
A.C. Forsberg ◽  
B.M. Stroebel ◽  
K.A. Faltesek ◽  
D.R. Verden ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Memory Loss ◽  
Insulin Pathway ◽  
Model Of Alzheimer’S Disease ◽  
Streptozotocin Rat Model
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