scholarly journals Neuroprotective Effect of Bean Phosphatidylserine on TMT-Induced Memory Deficits in a Rat Model

2020 ◽  
Vol 21 (14) ◽  
pp. 4901
Author(s):  
Minsook Ye ◽  
Bong Hee Han ◽  
Jin Su Kim ◽  
Kyungsoo Kim ◽  
Insop Shim
Keyword(s):  
Cognitive Function ◽  
Glucose Uptake ◽  
Rat Brain ◽  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Memory Deficits ◽  
Avoidance Task

Background: Trimethyltin (TMT) is a potent neurotoxin affecting various regions of the central nervous system, including the neocortex, the cerebellum, and the hippocampus. Phosphatidylserine (PS) is a membrane phospholipid, which is vital to brain cells. We analyzed the neuroprotective effects of soybean-derived phosphatidylserine (Bean-PS) on cognitive function, changes in the central cholinergic systems, and neural activity in TMT-induced memory deficits in a rat model. Methods: The rats were randomly divided into an untreated normal group, a TMT group (injected with TMT + vehicle), and a group injected with TMT + Bean-PS. The rats were treated with 10% hexane (TMT group) or TMT + Bean-PS (50 mg·kg−1, oral administration (p.o.)) daily for 21 days, following a single injection of TMT (8.0 mg/kg, intraperitoneally (i.p.)). The cognitive function of Bean-PS was assessed using the Morris water maze (MWM) test and a passive avoidance task (PAT). The expression of acetylcholine transferase (ChAT) and acetylcholinesterase (AchE) in the hippocampus was assessed via immunohistochemistry. A positron emission tomography (PET) scan was used to measure the glucose uptake in the rat brain. Results: Treatment with Bean-PS enhanced memory function in the Morris water maze (MWM) test. Consistent with the behavioral results, treatment with Bean-PS diminished the damage to cholinergic cells in the hippocampus, in contrast to those of the TMT group. The TMT+Bean-PS group showed elevated glucose uptake in the frontal lobe of the rat brain. Conclusion: These results demonstrate that Bean-PS protects against TMT-induced learning and memory impairment. As such, Bean-PS represents a potential treatment for neurodegenerative disorders, such as Alzheimer’s disease.

scholarly journals Reduced Cerebral Glucose Uptake in an Alzheimer’s Rat Model With Glucose-Weighted Chemical Exchange Saturation Transfer Imaging

2021 ◽  
Vol 13 ◽  
Author(s):  
Peidong Chen ◽  
Zhiwei Shen ◽  
Qianqian Wang ◽  
Bingna Zhang ◽  
Zerui Zhuang ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Chemical Exchange ◽  
Chemical Exchange Saturation Transfer ◽  
Control Group ◽  
Saturation Transfer ◽  
Nissl Staining ◽  
Brain Glucose

A correlation between the abnormal cerebral glucose metabolism and the progression of Alzheimer’s disease (AD) has been found in previous studies, suggesting that glucose alterations may be used to predict the histopathological diagnosis in AD. In this study, we investigated the dynamic changes of cerebral glucose uptake in vivo using MR glucose chemical exchange saturation transfer (glucoCEST) imaging in a rat model of AD with an intracerebroventricular (i.c.v) injection of amyloid Aβ-protein (25–35), confirmed by Morris water maze and Nissl staining. In total, 6 rats in the AD group and 6 rats in the control group that were given an injection of sterile normal saline were included. At 28 days after injection, all rats performed a 7.0 T MR exanimation, including glucoCEST, diffusion tensor imaging (DTI) and hippocampus magnetic resonance spectra (MRS), to detect the possible metabolic and structural changes in the rat brain. A significantly elevated brain glucoCEST signal in the brain of AD rats was observed, and a decreased brain glucose uptake was also explored during the progression of glucose infusion compared with those in rats of the control group. In addition, there is a significant positive correlation between glucoCEST enhancement (GCE) and myo-Inosito (Ins) in the AD group and the control group (P < 0.05). A significantly reduced number of neurons in the cortex and hippocampus in AD rats combined with the significantly longer escape and a decreased number of crossings were verified at 28 days after Aβ25–35 injection by Nissl staining and Morris water maze, respectively. Our results indicated that an abnormal brain glucose mechanism in AD rats could be detected by glucoCEST imaging, suggesting a new method to explore the occurrence and progress of diabetes-related AD or dementia.

scholarly journals SOLANUM BETACEUM IMPROVES COGNITIVE FUNCTION BY DECREASING N-METHYL-D-ASPARTATE ON ALZHEIMER RATS MODEL

2019 ◽  
pp. 167-170
Author(s):  
INDRI SAFITRI ◽  
HANIK BADRIYAH HIDAYATI ◽  
AGUS TURCHAN ◽  
SUHARTATI ◽  
SITI KHAERUNNISA
Keyword(s):  
Cognitive Function ◽  
Morris Water Maze ◽  
Water Maze ◽  
Memory Function ◽  
Drug Candidate ◽  
Enzyme Linked Immunosorbent Assay ◽  
Albino Rats ◽  
Assay Methods ◽  
Ethanol Extracts ◽  
Solanum Betaceum

Objective: The purpose of this study was to evaluate the effect of Solanum betaceum towards cognitive function, i.e. memory, and the level of N-Methyl-D-Aspartate receptor (NMDAR) and brain derived neurothropic factor (BDNF) as a drug candidate therapy for Alzheimer rats model.Methods: Fifty adult male albino rats were divided into five groups (K0, K1, P1, P2 and P3). Four groups (K1, P1, P2 and P3) of Alzheimer’s disease(AD) rats were induced by aluminum chloride with dose 2 g/L for 21 days period and three groups (P1, P2 and P3) in 22th day administered parallellywith 100 mg/kg b.w/day; 200 mg/kg b.w/day; and 400 mg/kg b.w/day of S. betaceum respectively for14 days. The level of NMDAR and BDNF wasmeasured by enzyme-linked immunosorbent assay methods, whereas memory was measured by the Morris water maze test.Results: S. betaceum administration increased cognitive function significantly (p=0.037) of AD induced-rats by decreasing the time to reach the targetof Morris water maze and maintaining the low levels of NMDAR significantly (p=0.006), but the level of BDNF did not increase significantly (p=0.346).These results indicated that ethanol extracts of S. betaceum could decrease brain NMDAR and increase cognitive function by promote better memoryfunction but did not significant increased the level of BDNF in AD-induced rats.Conclusion: This study revealed that the treatment of AD-induced rats with S. betaceum extracts significantly improve memory function and decreasethe level of NMDAR.

scholarly journals Acute pre-operative ibuprofen improves cognition in a rat model for postoperative cognitive dysfunction

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Klaske Oberman ◽  
Iris Hovens ◽  
Jacco de Haan ◽  
Joana Falcao-Salles ◽  
Barbara van Leeuwen ◽  
...  
Keyword(s):  
Cognitive Dysfunction ◽  
Morris Water Maze ◽  
Rat Model ◽  
Gut Microbiome ◽  
Water Maze ◽  
Single Injection ◽  
Postoperative Cognitive Dysfunction ◽  
Aged Rats ◽  
Short Term ◽  
Term Memory

Abstract Background Inflammation is considered a key factor in the development of postoperative cognitive dysfunction (POCD). Therefore, we hypothesized that pre-operative anti-inflammatory treatment with ibuprofen would inhibit POCD in our rat-model. Methods Male Wistar rats of 3 or 23 months old received a single injection of ibuprofen (15 mg/kg i.p.) or were control handled before abdominal surgery. Timed blood and fecal samples were collected for analyses of inflammation markers and gut microbiome changes. Behavioral testing was performed from 9 to 14 days after surgery, in the open field, novel object- and novel location-recognition tests and Morris water maze. Neuroinflammation and neurogenesis were assessed by immune histochemistry after sacrifice on postoperative day 14. Results Ibuprofen improved short-term spatial memory in the novel location recognition test, and increased hippocampal neurogenesis. However, these effects were associated with increased hippocampal microglia activity. Whereas plasma cytokine levels (IL1-β, IL6, IL10, and TNFα) were not significantly affected, VEGF levels increased and IFABP levels decreased after ibuprofen. Long-term memory in the Morris water maze was not significantly improved by ibuprofen. The gut microbiome was neither significantly affected by surgery nor by ibuprofen treatment. In general, effects in aged rats appeared similar to those in young rats, though less pronounced. Conclusion A single injection of ibuprofen before surgery improved hippocampus-associated short-term memory after surgery and increased neurogenesis. However, this favorable outcome seemed not attributable to inhibition of (neuro)inflammation. Potential contributions of intestinal and blood-brain barrier integrity need further investigation. Although less pronounced compared to young rats, effects in aged rats indicate that even elderly individuals could benefit from ibuprofen treatment.

scholarly journals Human Neural Stem Cells Encoding ChAT Gene Restore Cognitive Function via Acetylcholine Synthesis, Aβ Elimination, and Neuroregeneration in APPswe/PS1dE9 Mice

2020 ◽  
Vol 21 (11) ◽  
pp. 3958
Author(s):  
Dongsun Park ◽  
Ehn-Kyoung Choi ◽  
Tai-Hyoung Cho ◽  
Seong Soo Joo ◽  
Yun-Bae Kim
Keyword(s):  
Stem Cell ◽  
Cognitive Function ◽  
Memory Function ◽  
Memory Deficits ◽  
Therapeutic Approaches ◽  
Human Neural Stem Cells ◽  
Ache Inhibitors ◽  
Human Neural Stem Cell ◽  
Memory Acquisition ◽  
Ad Therapy

In Alzheimer disease (AD) patients, degeneration of the cholinergic system utilizing acetylcholine for memory acquisition is observed. Since AD therapy using acetylcholinesterase (AChE) inhibitors are only palliative for memory deficits without slowing or reversing disease progress, there is a need for effective therapies, and stem cell-based therapeutic approaches targeting AD should fulfill this requirement. We established a human neural stem cell (NSC) line encoding choline acetyltransferase (ChAT) gene, an acetylcholine-synthesizing enzyme. APPswe/PS1dE9 AD model mice transplanted with the F3.ChAT NSCs exhibited improved cognitive function and physical activity. Transplanted F3.ChAT NSCs in the AD mice differentiated into neurons and astrocytes, produced ChAT protein, increased the ACh level, and improved the learning and memory function. F3.ChAT cell transplantation reduced Aβ deposits by recovering microglial function; i.e., the down-regulation of β-secretase and inflammatory cytokines and up-regulation of Aβ-degrading enzyme neprilysin. F3.ChAT cells restored growth factors (GFs) and neurotrophic factors (NFs), and they induced the proliferation of NSCs in the host brain. These findings indicate that NSCs overexpressing ChAT can ameliorate complex cognitive and physical deficits of AD animals by releasing ACh, reducing Aβ deposit, and promoting neuroregeneration by the production of GFs/NFs. It is suggested that NSCs overexpressing ChAT could be a candidate for cell therapy in advanced AD therapy.

Edible Salt Plus D-Gal Accelerate Aging Progress

2014 ◽  
Vol 955-959 ◽  
pp. 326-334 ◽  
Author(s):  
Peng Wan ◽  
Cheng Xi Wei ◽  
Jian Long Wu ◽  
Qing Hua Jin
Keyword(s):  
Protein Expression ◽  
Spatial Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Memory Function ◽  
Accelerate Aging ◽  
Cox 2

Edible salt (ES) is also thought to exacerbate the symptoms of Alzheimer, however, the in vivo function of ES remains poorly understand. In this work, we investigated the phenomenon using the model of Alzheimer induced by D-gal. The behavious examination results exhibited that D-gal plus ES can weaken spatial memory function in the Morris water maze; the activities of T-SOD, GSH-Px and the CAT level in both hippocampus and cortex showed that D-gal plus ES decreased the expression of T-SOD and GSH-Px, but the expression of CAT increased, the protein expression determined in both of the hippocampus and cortex demonstrated that COX-2, iNOS, NFκ-B-p65-N proteins were significantly increased. It is possible that ES acts through several mechanisms, mediating a potential role in memory damage in mice. These results suggest that further study is necessary to evaluate the effect of salt on damage of memory and to determine the molecular mechanisms.

scholarly journals Surfactant reduction of cerebral infarct size and behavioral deficit in a rat model of cerebrovascular arterial gas embolism

2013 ◽  
Vol 115 (6) ◽  
pp. 868-876 ◽  
Author(s):  
David M. Eckmann ◽  
Stephen C. Armstead
Keyword(s):  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Decompression Sickness ◽  
Infarct Volume ◽  
Neurological Dysfunction ◽  
Morris Water Maze Test ◽  
Placement Test ◽  
Gas Embolism ◽  
Arterial Gas Embolism

Gas embolism occurs commonly in cardiac and vascular surgery and decompression sickness. The goals of this study were to develop a new in vivo rat model of cerebrovascular arterial gas embolism and to determine the effects of exogenous surfactants on resultant brain infarct volume and accompanying long-term neurological dysfunction using the model. Unilateral cerebral arterial gas embolism was induced in Sprague Dawley rats, including groups receiving intravenous Pluronic F-127 (PF-127) and Oxycyte perflourocarbon surfactant pretreatment. Magnetic resonance imaging (MRI) was performed at 24 and 72 h postembolism to determine infarct volume. The elevated body swing test (EBST), limb-placement test, proprioception forelimb and hindlimb tests, whisker tactile test, and Morris Water Maze test were performed to assess motor behavior, somatosensory deficit, and spatial cognitive function out to 29 days after embolization. A stable stroke model was developed with MRI examination revealing infarction in the ipsilateral cerebral hemisphere. Gas embolized rats had significant cognitive and sensorimotor dysfunction, including approximately threefold increase in Morris Water Maze latency time, ∼20% left-sided biasing in EBST performance, 0.5 to 1.5 (mean) point score elevations in the proprioception and whisker tactile tests, and 3.0 point (mean) elevation in the limb-placement test, all of which were persistent throughout the postembolic period. Surfactant prophylaxis with either PF-127 or Oxycyte rendered stroke undetectable by MRI scanning and markedly reduced the postembolic deficits in both cognitive and sensorimotor performance in treated rats, with normalization of EBST and whisker tactile tests within 7 days.

scholarly journals The Neuroprotective Effect of Methanol Extract ofGagamjungjihwanand Fructus Euodiae on Ischemia-Induced Neuronal and Cognitive Impairment in the Rat

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Bombi Lee ◽  
Eu-Jung Choi ◽  
Eun-Jung Lee ◽  
Seung-Moo Han ◽  
Dae-Hyun Hahm ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Learning And Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Methanol Extract ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Pre Treatment ◽  
And Performance ◽  
Cerebral Artery Occlusion

Gagamjungjihwan(GJ), a decoction consisting of five herbs includingginseng,Acori Graminei Rhizoma,Uncariae Ramulus et Uncus,Polygalae RadicandFrustus Euodiae(FE), has been widely used as herbal treatment for ischemia. In order to investigate the neuroprotective action of this novel prescription, we examined the influence of GJ and FE on learning and memory using the Morris water maze and studied their affects on the central cholinergic system in the hippocampus with neuronal and cognitive impairment. After middle cerebral artery occlusion was applied for 2 h, rats were administered GJ (200 mg kg−1, p.o.) or FE (200 mg kg−1, p.o.) daily for 2 weeks, followed by training and performance of the Morris water maze tasks. Rats with ischemic insults showed impaired learning and memory of the tasks. Pre-treatment with GJ and FE produced improvement in the escape latency to find the platform. Pre-treatments with GJ and FE also reduced the loss of cholinergic immunoreactivity in the hippocampus. The results demonstrated that GJ and FE have a protective effect against ischemia-induced neuronal and cognitive impairment. Our results suggest that GJ and FE might be useful in the treatment of vascular dementia.

scholarly journals Effect of Evodia rutaecarpa (Juss) Benth extract on Alzheimer disease in mice

2020 ◽  
Vol 19 (4) ◽  
pp. 823-828
Author(s):  
Ang Cai ◽  
Liu Xiao ◽  
Yan-Ping Zhou ◽  
Zhi-Guo Zhang ◽  
Quan-Wei Yang
Keyword(s):  
Cognitive Function ◽  
Alzheimer Disease ◽  
Water Maze ◽  
Memory Impairment ◽  
Escape Latency ◽  
Memory Deficits ◽  
Morris Water Maze Test ◽  
Maze Test ◽  
Evodia Rutaecarpa ◽  
Mouse Hippocampus

Purpose: To investigate the protective effect of Evodia rutaecarpa (Juss.) Benth. extract (ERBE) against Alzheimer's disease in 3xTg-AD mice. Methods: The cognitive function of 3xTg-AD mice was assessed using Morris water maze test. The levels of amyloid beta deposits and NeuN in the mouse hippocampus were evaluated by immunohistochemistry. Brain neurotrophic derived factor (BDNF) and tyrosine kinase B (TrkB) expressions were determined by western blot analysis. Results: ERBE treatment significantly ameliorated learning and memory deficits in AD mice, as shown by increased time spent in the target zone during probe tests. The escape latency in the animals treated with 400 mg/kg ERBE (20.5 ± 1.3 s) was significantly higher than untreated 3xTg-AD mice (12.4 ± 1.3 s, p < 0.01). In addition, ERBE significantly decreased Aβ deposits, increased NeuN-positive cells, and upregulated the expressions of BDNF (1.4 ± 0.2, p < 0.05) and TrkB (1.1 ± 0.2, p < 0.05) in 3xTg AD mice. Conclusion: The results suggest that ERBE administration may be a useful strategy for treating memory impairment induced by several neurodegenerative diseases. Keywords: Evodia rutaecarpa, Alzheimer, Memory impairment, NeuN-positive cells

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