scholarly journals Effect of Streblus asper Leaf Extract on Scopolamine-Induced Memory Deficits in Zebrafish: The Model of Alzheimer’s Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Kanathip Singsai ◽  
Natthanicha Ladpala ◽  
Natthan Dangja ◽  
Thanyaret Boonchuen ◽  
Niracha Jaikhamfu ◽  
...  

Streblus asper (SA) is well known as a folk medicinal plant in Asian countries. The effect of SA extract on preventing memory impairment in zebrafish induced by scopolamine was investigated. Male zebrafish, Danio rerio, were divided into 6 groups including the control, scopolamine 200 μM (SCO), scopolamine plus rivastigmine 1.5 mg/kg (RV + SCO), and scopolamine plus SA extract at doses of 200, 400, and 800 mg/kg (SA200 + SCO, S400 + SCO, and SA800 + SCO), respectively. Spatial memory was evaluated by the colour-biased appetite conditioning T-maze test, while fear memory was measured by the inhibitory avoidance test. In the spatial memory test, results showed that the RV + SCO group had the best time spent ratio in the T-maze, followed by SA800 + SCO, SA400 + SCO, SA200 + SCO, control, and SCO group, respectively, but with no statistical significance. For the fear memory test, zebrafish that received SA at doses of 200, 400, and 800 mg/kg had significantly increased latency time as 21.75 ± 4.59, 23.75 ± 13.01, and 18.20 ± 18.84 min, respectively, when compared to the SCO group (9.80 ± 10.45 min). These results suggested that SA extract attenuated memory impairment in an inhibitory avoidance test related to fear memory. Our findings can be useful for further research to develop SA extract as a health product to ameliorate the symptoms of Alzheimer’s disease.

2017 ◽  
Vol 4 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Hiroshi Moriyama ◽  
Takuya Watanabe ◽  
Kotaro Takasaki ◽  
Masaki Nagao ◽  
Kaori Kubota ◽  
...  

2002 ◽  
Vol 50 (6) ◽  
pp. 1086-1091 ◽  
Author(s):  
Gail Kuslansky ◽  
Herman Buschke ◽  
Mindy Katz ◽  
Martin Sliwinski ◽  
Richard B. Lipton

2020 ◽  
Vol 9 (1) ◽  
pp. 17
Author(s):  
Ebrahim Esfandiari ◽  
Zeinab Shakerin ◽  
Shahnaz Razavi ◽  
Hojjatallah Alaei ◽  
Mustafa Ghanadian ◽  
...  

Author(s):  
Ana E. Gonçalves ◽  
Ângela Malheiros ◽  
Camila A. Cazarin ◽  
Lara de França ◽  
David L. Palomino-Salcedo ◽  
...  

Background: Chalcones and dihydrochalcones present potent inhibition of acetylcholinesterase, which is currently considered the most efficient approach for symptomatic treatment of Alzheimer’s disease. Objective: The present study aimed to explore the potential benefits of 2',6'-dihydroxy-4'-methoxy dihydrochalcone on the cognitive deficits of animals submitted to the streptozotocin-induced Alzheimer's model, as well as to evaluate the possible mechanisms of action. Methods: Learning and memory functions of different groups of animals were submitted to the streptozotocin-induced Alzheimer's model (STZ 2.5 mg/mL, i.c.v.) and subsequently treated with 2',6'-dihydroxy-4'-methoxy dihydrochalcone (DHMDC) administered at doses 5, 15, and 30 mg/kg (p.o.), rivastigmine (0,6 mg/kg, i.p.) and vehicle were evaluated in aversive memory test (inhibitory avoidance test) and spatial memory test (object recognition test). Molecular docking simulations were performed to predict the binding mode of DHMDC at the peripheral site of AChE to analyze noncovalent enzyme-ligand interactions. DFT calculations were carried out to study well-known acetylcholinesterase inhibitors and DHMDC. Results: DHMDC markedly increased the learning and memory of mice. STZ caused a significant decline of spatial and aversive memories in mice, attenuated by DHMDC (15 and 30 mg/kg). Furthermore, STZ conspicuously increased lipid peroxidation and compromised the antioxidant levels in mice brains. DHMDC pretreatment significantly increased GSH activity and other oxidative stress markers and decreased TBARS levels in the brain of STZ administered mice. AChE activity was significantly decreased by DHMDC in the brain of mice. Conclusion: The results together point that DHMDC may be a useful drug in the management of dementia.


Author(s):  
Mohammad Mehdipour ◽  
Masoumeh Emamghoreishi ◽  
Majid Reza Farrokhi ◽  
Elahe Amirinezhadfard ◽  
Mojtaba Keshavarz

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.


2019 ◽  
Author(s):  
Emily A. Jones ◽  
Anna K. Gillespie ◽  
Seo Yeon Yoon ◽  
Loren M. Frank ◽  
Yadong Huang

SUMMARYAlzheimer’s disease (AD) is characterized by progressive memory loss, and there is a pressing need to identify early pathophysiological alterations that predict subsequent memory impairment. Hippocampal sharp-wave ripples (SWRs) – electrophysiological signatures of memory reactivation in the hippocampus – are a compelling candidate for doing so. Mouse models of AD show reductions in both SWR abundance and associated slow gamma (SG) power during aging, but these alterations have yet to be directly linked to memory impairments. In aged apolipoprotein E4 knock in (apoE4-KI) mice – a model of the major genetic risk factor for AD – we found that reduced SWR abundance and associated CA3 SG power predicted spatial memory impairments measured 1–2 months later. Importantly, SWR-associated CA3 SG power reduction in young apoE4-KI mice also predicted spatial memory deficits measured 10 months later. These results establish features of SWRs as potential functional biomarkers of memory impairment in AD.


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