The neuroprotective effects of flupirtine and beta-amyloid induced memory impairment

2011 ◽  
Author(s):  
Matthew Jefferson ◽  
Sara Smeltzer ◽  
Jeffery L. McMillin ◽  
Caitlin C. Henry ◽  
Brittney M. Klauser ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Beta Amyloid ◽  
Neuroprotective Effects

β-1, 3-Glucan attenuated chronic unpredictable mild stress induced cognitive impairment in rodents via normalizing corticosterone levels

2020 ◽  
Vol 20 ◽  
Author(s):  
Saniya Hashim Khan ◽  
Sheraz Khan ◽  
Inamullah Khan ◽  
Narmeen Hashim
Keyword(s):  
Water Maze ◽  
Memory Impairment ◽  
Glucocorticoid Receptors ◽  
Therapeutic Potential ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Neuroprotective Effects ◽  
Injurious Effect ◽  
Naturally Occurring ◽  
Dose Dependent

Background: Chronic stress elevates the cortisol beyond normal levels, which affects cognition including learning & memory. This injurious effect is primarily mediated via over excitation of metabotropic glucocorticoid receptors (mGR). Methods: The present study was aimed appraise the neuroprotective effects of naturally occurring molecule β-1,3-glucan by interfering with stress-cortisol-mGR axis. Our data of virtual screening (in silico) exhibited the promising interactions of βglucan with the mGR. Therefore, the study was extended to evaluate its efficacy (2.5, 5 and 10 mg/kg/ i.p) in an animal model of chronic unpredictable mild stress (CUMS, 28 days) induced memory impairment. Results: Results of the current study revealed the β-glucan provided dose dependent protection against deleterious effects of stress on learning and memory associated parameters observed in Morris water maze (MWM) task. At higher tested doses, it has also significantly antagonized the stress induced weight loss and corticosterone elevation. Conclusion: From these findings, it can be deduced that the β-glucan possesses therapeutic potential against stress induced memory impairment, and this effect can be attributed to its normalizing effect on corticosterone levels.

Neuroprotective effects of sigma-1 receptor agonists against beta-amyloid-induced toxicity

Neuroreport ◽  
2005 ◽  
Vol 16 (11) ◽  
pp. 1223-1226 ◽  
Author(s):  
Agostino Marrazzo ◽  
Filippo Caraci ◽  
Elisa Trovato Salinaro ◽  
Tsung-Ping Su ◽  
Agata Copani ◽  
...  
Keyword(s):  
Beta Amyloid ◽  
Neuroprotective Effects ◽  
Sigma 1 Receptor ◽  
Receptor Agonists ◽  
Sigma 1

Piper sarmentosum Roxb. Attenuates Beta Amyloid (Aβ)-Induced Neurotoxicity Via the Inhibition of Amyloidogenesis and Tau Hyperphosphorylation in SH-SY5Y Cells

2021 ◽  
Vol 18 (1) ◽  
pp. 80-87
Author(s):  
Elaine W.L. Chan ◽  
Emilia T.Y. Yeo ◽  
Kelly W.L. Wong ◽  
Mun L. See ◽  
Ka Y. Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Beta Amyloid ◽  
Mechanistic Study ◽  
Tau Hyperphosphorylation ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Hexane Extracts ◽  
Anti Oxidant ◽  
Amyloid Aβ

Background: In Alzheimer’s disease, accumulation of beta amyloid (Aβ) triggers amyloidogenesis and hyperphosphorylation of tau protein leading to neuronal cell death. Piper sarmentosum Roxb. (PS) is a traditional medicinal herb used by Malay to treat rheumatism, headache and boost memory. It possesses various biological effects, such as anti-cholinergic, anti-inflammatory, anti-oxidant and anti-depressant-like effects. Objective: The present study aimed to investigate neuroprotective properties of PS against Aβ-induced neurotoxicity and to evaluate its potential mechanism of action. Methods: Neuroprotective effects of hexane (HXN), dichloromethane (DCM), ethyl acetate (EA) and methanol (MEOH) extracts from leaves (L) and roots (R) of PS against Aβ-induced neurotoxicity were investigated in SH-SY5Y human neuroblastoma cells. Cells were pre-treated with PS for 24 h followed by 24 h of induction with Aβ. The neuroprotective effects of PS were studied using cell viability and cellular reactive oxygen species (ROS) assays. The levels of extracellular Aβ and tau proteins phosphorylated at threonine 231 (pT231) were determined. Gene and protein expressions were assessed using qRT-PCR analyses and western blot analyses, respectively. Results: Hexane extracts of PS (LHXN and RHXN) protected SH-SY5Y cells against Aβ-induced neurotoxicity, and decreased levels of extracellular Aβ and phosphorylated tau (pT231). Although extracts of PS inhibited Aβ-induced ROS production, it was unlikely that neuroprotective effects were simply due to the anti-oxidant capacity of PS. Further, mechanistic study suggested that the neuroprotective effects of PS might be due to its capability to regulate amyloidogenesis through the downregulation of BACE and APP. Conclusion: These findings suggest that hexane extracts of PS confer neuroprotection against Aβ- induced neurotoxicity in SH-SY5Y cells by attenuating amyloidogenesis and tau hyperphosphorylation. Due to its neuroprotective properties, PS might be a potential therapeutic agent for Alzheimer’s disease.

Neuroprotective effects of thymoquinone against MDMA-induced neurotoxicity

2021 ◽  
pp. 5945-5952
Author(s):  
Mustafa NS. ◽  
Mohamad N. ◽  
Abu Bakar NH. ◽  
Mohd Adnan LH. ◽  
Jeharsae R. ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Natural Compound ◽  
Neuronal Damage ◽  
Memory Performance ◽  
Novel Object Recognition ◽  
Psychoactive Substance ◽  
Sprague Dawley ◽  
Hippocampal Dentate Gyrus ◽  
Object Recognition Test ◽  
Neuroprotective Effects

MDMA (3, 4-methylenedioxymethamphetamine) is a psychoactive substance that is associated with neurotoxicity. MDMA exposure to human results in the degeneration of neuronal cells in the hippocampus. Hence, the purpose of this study was to examine the potential of a natural compound known as thymoquinone (TQ) to protect against neuronal damage and memory impairment in rats stimulated by MDMA. The administration of TQ into MDMA-induced neuronal damage rats was carried out in male Sprague Dawley via a 1-week treatment dividing into four groups (n=36, 7-9 per group). The studied groups involved with the treatments comprise i) Control (1 mL/kg saline), ii) MDMA (10 mg/kg MDMA), iii) MDMA+TQ (10 mg/kg MDMA + 40 mg/kg TQ) and iv) TQ control (40 mg/kg TQ). A novel object recognition test (NORT) was carried out to evaluate the memory performance of the rats, followed by a histopathological assessment of the hippocampal dentate gyrus. The histopathology analysis revealed a significant increase in numbers of positive cells by Fluoro-Jade C following the effect of MDMA on neuronal damage (MDMA induced group) compared to control (P<0.05). Next, the TQ treatments observed in MDMA+TQ exhibited a decline in positive cells from Fluoro-Jade C. The index of recognition memory was found to be increased in MDMA+TQ compared to the MDMA alone (P<0.05). This study suggests that the neuronal damage inflicted by MDMA in a rat model has the potential to be treated by TQ.

scholarly journals M5. Beta Amyloid Level is not Elevated in Elderly Patients With Schizophrenia: Are There Potential Neuroprotective Effects of Antipsychotics on Beta-Amyloid Pathology?

2017 ◽  
Vol 43 (suppl_1) ◽  
pp. S212-S212
Author(s):  
Jun Ku Chung ◽  
Shinichiro Nakajima ◽  
Eric Plitman ◽  
Fernando Caravaggio ◽  
Philip Gerretsen ◽  
...  
Keyword(s):  
Elderly Patients ◽  
Beta Amyloid ◽  
Neuroprotective Effects ◽  
Amyloid Pathology

Neuroprotective effects of pretreatment with minocycline on memory impairment following cerebral ischemia in rats

2017 ◽  
Vol 28 ◽  
pp. 214-222 ◽  
Author(s):  
Yazdan Naderi ◽  
Masoumeh Sabetkasaei ◽  
Siavash Parvardeh ◽  
Taraneh Moini Zanjani
Keyword(s):  
Cerebral Ischemia ◽  
Memory Impairment ◽  
Neuroprotective Effects

scholarly journals Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

2018 ◽  
Vol 46 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Ting-Ting Xu ◽  
Yang Zhang ◽  
Jia-Yang He ◽  
Dan Luo ◽  
Yi Luo ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blotting ◽  
Disease Model ◽  
Beta Amyloid ◽  
Amyloid Peptide ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Y Maze ◽  
Improved Learning

Background/Aims: Alzheimer disease (AD) is a common neurodegenerative disease that is characterized by the deposition of beta-amyloid peptide and formation of intracellular neurofibrillary tangles. Due to the failure of various clinical trials of novel drugs for AD, effective drugs for AD treatment are urgently required. Methods: In this study, we used the classic APP/PS1 mouse model to explore the neuroprotective effects of a new compound, bajijiasu, and the mechanisms involved. Behavioral tests and western blotting were performed to assess the beneficial effects of bajijiasu in APP/PS1 mice. Results: Morris water maze and Y-maze test results showed that oral administration of bajijiasu (35 mg/kg/day and 70 mg/kg/day) improved learning and memory abilities in APP/PS1 mice. Bajijiasu reduced ROS and MDA levels in both the hippocampus and cortex. Moreover, western blotting results showed that bajijiasu protected neurons from apoptosis, elevated the expression levels of neurotrophic factors, and alleviated endoplasmic reticulum stress in both the hippocampus and cortex. Conclusion: These results indicate that the mechanisms underlying the effects of bajijiasu on AD might be related to beta-amyloid-downstream pathologies, particularly endoplasmic reticulum stress.

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