Chronic Lithium Treatment in a Rat Model of Basal Forebrain Cholinergic Depletion: Effects on Memory Impairment and Neurodegeneration

2017 ◽  
Vol 56 (4) ◽  
pp. 1505-1518 ◽  
Author(s):  
Francesca Gelfo ◽  
Debora Cutuli ◽  
Annalisa Nobili ◽  
Paola De Bartolo ◽  
Marcello D’Amelio ◽  
...  
Keyword(s):  
Rat Model ◽  
Basal Forebrain ◽  
Memory Impairment ◽  
Lithium Treatment

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 ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Sleep Disturbance ◽  
Rat Model ◽  
Memory Impairment ◽  
Ameliorative Effect

scholarly journals Effect of chemogenetic modulation of hippocampal neurons on depression and spatial memory impairment in a rat model for temporal lobe epilepsy.

2019 ◽  
Vol 13 ◽  
Author(s):  
Erine Craey ◽  
Marie-Gabrielle Goossens ◽  
Jana Desloovere ◽  
Caroline Merckx ◽  
Chris Van Den Haute ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Spatial Memory ◽  
Temporal Lobe ◽  
Rat Model ◽  
Hippocampal Neurons ◽  
Memory Impairment

Novel Therapeutic Mechanism of Action of Metformin and Its Nanoformulation in Alzheimer's Disease and Role of AKT/ERK/GSK Pathway.

2021 ◽  
Author(s):  
Harish Kumar ◽  
Amitava Chakrabarti ◽  
Phulen Sarma ◽  
Manish Modi ◽  
Dibyajyoti Banerjee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Control ◽  
Rat Model ◽  
Memory Impairment ◽  
Protective Efficacy ◽  
Control Group ◽  
Hyperphosphorylated Tau ◽  
Days Of Therapy

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.

scholarly journals Omega-3 Fatty Acids Prevent Post-Traumatic Stress Disorder-Induced Memory Impairment

Biomolecules ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 100 ◽  
Author(s):  
Laiali Alquraan ◽  
Karem H. Alzoubi ◽  
Hana Hammad ◽  
Suzie Y. Rababa’h ◽  
Fadia Mayyas
Keyword(s):  
Fatty Acids ◽  
Rat Model ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Impairment ◽  
Stress Disorder ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Post Traumatic Stress ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that can happen after exposure to a traumatic event. Post-traumatic stress disorder is common among mental health disorders that include mood and anxiety disorders. Omega-3 fatty acids (OMGs) are essential for the maintenance of brain function and prevention of cognition dysfunctions. However, the possible effect of OMG on memory impairment induced by PTSD has not been studied. In here, such an effect was explored using a rat model of PTSD. The PTSD-like behavior was induced in animals using a single-prolonged stress (SPS) rat model of PTSD (2 h restraint, 20 min forced swimming, 15 min rest, 1–2 min diethyl ether exposure). The OMG was administered orally at a dose of 100 mg omega-3 polyunsaturated fatty acid (PUFA)/100 g body weight/day. Spatial learning and memory were assessed using the radial arm water maze (RAWM) method. Changes in oxidative stress biomarkers, thiobarbituric acid reactive substances (TBARS), and brain derived neuroptrophic factor (BDNF) in the hippocampus following treatments were measured. The results revealed that SPS impaired both short- and long-term memory (p < 0.05). Use of OMG prevented memory impairment induced by SPS. Furthermore, OMG normalized SPS induced changes in the hippocampus that reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratios, the activity of catalase, glutathione peroxidase (GPx), and TBARSs levels. In conclusion, the SPS model of PTSD-like behavior generated memory impairment, whereas OMG prevented this impairment, possibly through normalizing antioxidant mechanisms in the hippocampus.

scholarly journals Hwangryunhaedok-Tang Exerts Neuropreventive Effect on Memory Impairment by Reducing Cholinergic System Dysfunction and Inflammatory Response in a Vascular Dementia Rat Model

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 343 ◽  
Author(s):  
Eunjin Sohn ◽  
Yu Kim ◽  
Hye-Sun Lim ◽  
Bu-Yeo Kim ◽  
Soo-Jin Jeong
Keyword(s):  
Vascular Dementia ◽  
Rat Model ◽  
Memory Impairment ◽  
Neuronal Damage ◽  
Inflammatory Diseases ◽  
Ethanol Extract ◽  
Mitogen Activated Protein Kinase ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Cholinergic Dysfunction

Hwangryunhaedok-tang (HRT) is a traditional oriental herbal formula used in Asian countries for treating inflammatory diseases and controlling fever. Our present study aimed to determine whether HRT has therapeutic effects for patients with vascular dementia (VaD) using a bilateral common carotid artery occlusion (BCCAO) rat model and assessing spatial memory impairment and activation of neuroinflammation. BCCAO was performed in male Sprague Dawley rats to induce VaD, and oral HRT was administered daily for 30 d. Our data showed that HRT ameliorated BCCAO-induced memory and cognitive impairment in behavioral tests. In addition, HRT reversed cholinergic dysfunction and neuronal damage in the hippocampus of BCCAO rats. Furthermore, HRT attenuated microglial activation and reduced the phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK) induced by BCCAO. Simultaneous high-performance liquid chromatography analysis of HRT using index compounds from the herbal composition revealed that both HRT ethanol extract and commercial HRT granules primarily comprise geniposide, baicalin, and berberine. Our study showed that HRT administration resulted in the prevention of neuronal injury induced by BCCAO through improvement of cholinergic dysfunction and inhibition of neuroinflammatory responses, suggesting that HRT may have potential as a treatment for VaD.

Caffeine Consumption Prevents Memory Impairment, Neuronal Damage, and Adenosine A2A Receptors Upregulation in the Hippocampus of a Rat Model of Sporadic Dementia

2013 ◽  
Vol 34 (2) ◽  
pp. 509-518 ◽  
Author(s):  
Janaína Espinosa ◽  
Andreia Rocha ◽  
Fernanda Nunes ◽  
Marcelo S. Costa ◽  
Vanessa Schein ◽  
...  
Keyword(s):  
Rat Model ◽  
Memory Impairment ◽  
Neuronal Damage ◽  
Adenosine A2a Receptors ◽  
Caffeine Consumption ◽  
A2a Receptors ◽  
Adenosine A2a

Neurotoxic effects of high-dose piperine on hippocampal synaptic transmission and synaptic plasticity in a rat model of memory impairment

2020 ◽  
Vol 79 ◽  
pp. 200-208 ◽  
Author(s):  
Masoomeh Nazifi ◽  
Manoochehr Ashrafpoor ◽  
Shahrbanoo Oryan ◽  
Delaram Eslimi Esfahani ◽  
Ali Akbar Moghadamnia
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Rat Model ◽  
Memory Impairment ◽  
High Dose ◽  
Neurotoxic Effects
Sign in / Sign up

Export Citation Format

Share Document