Ameliorative effect of sansoninto on sleep disturbance and spatial memory impairment in an Alzheimer's disease rat model

2017 ◽  
Vol 4 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Hiroshi Moriyama ◽  
Takuya Watanabe ◽  
Kotaro Takasaki ◽  
Masaki Nagao ◽  
Kaori Kubota ◽  
...  
2020 ◽  
Vol 9 (1) ◽  
pp. 17
Author(s):  
Ebrahim Esfandiari ◽  
Zeinab Shakerin ◽  
Shahnaz Razavi ◽  
Hojjatallah Alaei ◽  
Mustafa Ghanadian ◽  
...  

2021 ◽  
Author(s):  
Samaneh Safari ◽  
Naser Mirazi ◽  
Nesa Ahmadi ◽  
Masoumeh Asadbegi ◽  
Alireza Nourian ◽  
...  

Abstract Alzheimer's disease (AD) as a neurodegenerative disease is recognized with progressive cognitive function failure, which is determined by beta-amyloid (Aβ) accumulation in extracellular space and hyperphosphorylation of intracellular Tau protein. Aβ stimulates some kinds of active oxygen and causes oxidative stresses and apoptosis. Policosanol (PCO) is a reducing lipid complement, which has antioxidant and anti-inflammatory activities. In the current research, the PCO effects on learning and memory impairment were investigated in a rat model of AD. Healthy adult male Wistar rats (230–250g) were divided randomly into 7 groups (n=6-7): Control, Sham (5 µL of phosphate-buffered saline, intracerebroventricular (ICV) microinjection), AD model (5 µL, ICV injection of Aβ), acacia gum (50 mg/kg, 8 weeks, gavage), PCO (50 mg/kg, 8 weeks, gavage), AD + acacia gum (50 mg/kg, 8 weeks, gavage), and AD + PCO (50 mg/kg, 8 weeks, gavage). Passive avoidance learning (PAL) and memory were assessed by shuttle box, cognitive memory by novel object recognition (NOR), and spatial memory by the Morris water maze (MWM) test. The oxidant and antioxidant parameters were examined at the end of the experiments. According to our results, ICV injection of Aβ caused reduced cognitive memory in NOR, spatial memory in MWM, and passive avoidance in PAL tests. PCO caused a recovery in cognitive memory, spatial memory, and PAL memory. Aβ plaques increased in the AD group, while PCO decreased it. Aβ increased total oxidant status and decreased total antioxidant capacity, whereas PCO reversed these parameters. Our results demonstrated that PCO has neuroprotective effects and can protect learning and memory impairments via its hypolipidemic and antioxidant effects.


2021 ◽  
Author(s):  
Harish Kumar ◽  
Amitava Chakrabarti ◽  
Phulen Sarma ◽  
Manish Modi ◽  
Dibyajyoti Banerjee ◽  
...  

Abstract Background: Insulin resistance in brain plays a critical role in the pathogenesis of Alzheimer's disease (AD). Metformin is a blood brain barrier crossing anti-diabetic insulin-sensitizer drug. Current study has evaluated the therapeutic and mechanistic role of conventional as well as solid lipid nanoformulation (SLN) of metformin in intracerebro ventricular (ICV) Aβ (1-42) rat-model of AD. Methods: SLN-metformin was prepared by the micro-emulsification method and further evaluated by zetasizer and scanning electron-microscopy. In the animal experimental phase, AD was induced by bilateral ICV injection of Aβ using stereotaxic technique, whereas control group (sham) received ICV-NS. 14 days post-model induction, ICV- Aβ treated rats were further divided into 5 groups: disease control (no treatment), Metformin dose of (50mg/kg, 100mg/kg and 150 mg/kg), SLN of metformin 50mg/kg and memantine 1.8mg/kg (positive-control). Animals were tested for cognitive performance (in EPM, MWM) after 21 days of therapy, and then sacrificed. Brain homogenate was evaluated using ELISA for (Aβ (1-42), hyperphosphorylated tau, pAKTser473, GSK-3β, p-ERK,) and HPLC (metformin level). Brain histopathology was used to evaluate neuronal injury score (H&E) and Bcl2 and BAX (IHC). Results: The average size of SLN-metformin was <200 nm and was of spherical in shape with 94.08% entrapment efficiency. Compared to sham, the disease-control group showed significantly higher (p≤0.05) memory impairment (in MWM and EPM), higher hyperphosphorylated tau, Aβ (1-42), and Bax and lower Bcl-2 expression. Metformin was detectable in brain. Treatment with metformin and its SLN form significantly decreased the memory impairment as well as decreased the expression of hyperphosphorylated tau, Aβ(1-42), Bax expression and increased expression of Bcl-2 in brain. AKT-ERK-GSK3β-Hyperphosphorylated tau pathway can be implicated in the protective efficacy of metformin. Conclusion: Both metformin and SLN metformin is found to be effective as therapeutic agent in ICV-AB rat model of AD. AKT-ERK-GSK3β-Hyperphosphorylated tau pathway is found to be involved in the protective efficacy of metformin.


Author(s):  
Jamileth More ◽  
Nadia Galusso ◽  
Pablo Veloso ◽  
Luis Montecinos ◽  
José Pablo Finkelstein ◽  
...  

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