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Introduction: One of the most common markers in Alzheimer’s disease (AD) is amyloid beta (Aβ) plaques. Anti-inflamm-atory agents including phagocytosis by immune cells, proteolytic enzymes and liver are known to decline the risk of Aβ plaques formation. In the previous study we showed that aqueous extract of Lavandula angusti-folia (lavender) improved memory deficits in Alzheimeric rats. Here, we evaluated ef-fect of the lavender extract on the clearance of Aβ plaques in the hippocampus. Materials & Methods: The animal model of Alzheimer was created with the injection of Aβ 1-42 fragment into the cerebroven-tricular space of brain. The brain sections were stained using Congo red to confirm formation of Aβ plaques. Twenty days after injection of Aβ 1-42 fragment, the animals received different doses (50, 100 and 200 mg/kg) of the aqueous extract of lavender for a period of 20 days. Findings: Our results showed that 50 mg/kg of lavender extract did not effectively influence the Aβ plaques. On the other hand, the doses of 100 and 200 mg/kg of the herbal medicine markedly decreased the extent of Aβ aggregates. The higher con-centration was more effective. Discussion & Conclusion: The lavender extract eliminates Aβ plaques in a dose dependent manner. The exact mechanism by which the herbal medicine removes the Aβ aggregates needs to be elucidated.

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: One of the shortcuts to disco-ver drug targets is the utilizing of new kn-owledge of basic medical sciences such as genomics, proteomics, metabolomics, bio-informatics and biostatistics that are apply-ing holistic approaches to study biological and medical subjects. In this study pro-teomics, bioinformatics and biostatistics techniques were applied to identify prob-able therapeutic proteins targets for the treatment of Alzheimer's disease. Hippoc-ampus proteomes of normal and Alzhe-imeric rats treated with aqueous extract of lavender were evaluated with protein expr-ession clustering method. Materials & Methods: Proteins of hippoc-ampus samples from normal and Alzheim-eric rats that treated with aqueous extract of lavender (CE and AE) and without the extract (C and A) were extracted. Proteins were separated by using of two-dimensional gel electrophoresis and the gels were stai-ned by silver staining methods. Bioinfo-rmatics and biostatistics analysis of the separated were accomplished by bioinfo-rmatics software. Findings: Bioinformatics and statistical analysis of the stained gels obtained 990 proteins in the four groups of rats. Prote-omic comparison of A and AE groups reve-aled that the expression of 49 proteins was inhibited, while the expression of 26 new proteins in the AE group was observed that may be due to the present of lavender extract. Proteomic comparison between gro-ups C and CE showed the expression of the 80 new proteins and inhibition of 104 pro-teins. Discussion & Conclusion: After the remov-al of common proteins between the two groups, those proteins that were affected by the extract assigned as drug targets for the treatment of Alzheimer. Changes at the molecular level were revealed with multi-variate statistical analyzes such as principal component analysis or correlation analysis and the clustering of proteins showed that the expression changes have been occurred in three main clusters. Finally, it could be concluded that lavender extract caused significant expression changes in the pro-teome and possibly activated specific biological processes in the rats’ hippoc-ampus that associated with enhancement of learning and memory in normal and Alzh-eimeric rats.

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Introduction: benzodiazepine drugs notably have an anxiolytic and amnesic features, while β-carbolines as their receptors inverse agonists show effects of anxiety and increasing learning features. The aim of present study was to investigate the effects of Norharmane on memory retention of Alzheimer model rats induced with streptozotocin (STZ) in passive avoidance learning.
 Materials & methods: 48 male wistar rats were divided into: control, STZ, STZ+ alcohol and STZ+ norharmane groups. STZ was injected bilaterally into lateral ventricles for induction of AD, (3 mg/kg, i.c.v, 10 μl on each side). Two weeks later, all rats were trained in the passive avoidance device (50Hz, 1mA, for 3sec). Alcohol (0.2ml) or Norharmane (1, 2, 4 mg/kg, Intraperitoneal) were injected to rats after training immediately. Retention test was done 48 hours later. The time to take the animal enters the dark chamber device measured as a standard memory.
 Findings: Injection of Norharmane in low dose (1, 2 mg/kg) after training improve memory retention in Alzheimer's rats while Norharmane in high dose (4 mg/kg) lead to further impairment of memory retention in Alzheimer's rats of streptozotoc model. So that presence time in the light area before entering to dark area in the STZ+norharmane (2 mg/kg) group were significantly higher than STZ group (P<0.05).
 Discussion & Conclusion: According to findings, Norharmane, as inverse agonists of benzodiazepine receptors in low doses may be useful through stimulation GABA receptors for Alzheimer's disease treatment.

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Introduction: Alzheimer's disease (AD) is one of the neurodegenerative diseases which is associated with cognitive, behavior and motoral impairments. The main symptom of this disease is dementia, which may cause difficulties in carrying out daily practices. According to multifactorial nature of the disease and its several causing factors, studies have raised the hypothesis that serum levels of some metals may be involved in causing of AD. One of these metals is aluminum. The aim of this study was to evaluate aluminum levels in Alzheimer patient's serum with severity of disease on one hand and comparing it in patients and healthy individuals on the other hand.

Materials & methods: In this study a group of patients with a definite diagnosis of Alzheimer's disease were assessed with Global Deterioration Scale (GDS) for severity of illness. The amount of aluminum in serum was measured by atomic absorption spectrophotometry in each patient and control groups. The relationship between the aluminum and the severity of disease was examined.

Findings: 50 patients (26 male / 24 female) and 50 healthy subjects (29 male / 21 female) were enrolled in the study. Serumic Aluminum levels in patients and controls were 37.17± 17ug/L and 23.38±30 ug/L respectively (p= 0.006). Also the serumic aluminum was significantly associated with severity of disease (r = 0.913 and p< 0.001).

Discussion & Conclusions: The study indicated that significant differences of the serumic Aluminum levels between Alzheimer's disease and normal subjects and Aluminum can be raised as a environmental factor in causing & severity of AD.

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Introduction: Alzheimer's disease is the most common neurodegenerative disorder. Due to the neurodegenerative effect of fennel (Foeniculum vulgare) this study aimed at investigating the effect of this plant on the improvement of learning and memory in rat models of Alzheimer's disease. 

Material & Methods: The male Wistar rats were assigned into six groups, namely the control group (no injection), sham group (saline injection), experimental group (injection of beta-amyloid (40-1). The other three groups received 75, 140, and 250 ml/kg of fennel extract intraperitoneally 7 days before and 3 weeks after bilateral intraventricular beta-amyloid injection. Shuttle box was used to study the learning and memory behavior of the rats; moreover hematoxylin-eosin staining was conducted for histological studies.

Findings: According to the results, fennel extract at a dose of 140 mg/kg increased behavioral indicators in measuring the passive avoidance memory in the Alzheimer's group, compared to the sham group (P<0.001). Moreover, optical microscopy studies showed a significant decrease in tissue damage and an increase in the number of Nissl bodies stained in CA1 hippocampal region, especially in pyramidal layer, in Alzheimer's disease-induced rats treated with fennel extract at a dose of 140 mg/kg.

Discussion & Conclusions: In this study, fennel extract shows the neuroprotective effect against Alzheimer’s disease induced by beta-amyloid (40-1). the observed improvements are probably related with antioxidant, anti-inflammatory, and pseudo-estrogenic properties of this plant. 

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Introduction: Stem cell-based therapies create new hope for the treatment of Alzheimer's disease (AD). Since the mesenchymal stem cells have neuroprotective and regeneration effects, this study aimed to investigate the memory, learning, and antioxidant capacity of the hippocampus following human adipose-derived mesenchymal stem cell (Ad-MSC) transplantation in Trimethyltin (TMT) rat's model of AD.
Material & Methods: In total, 24 male Wistar rats were randomly divided into three groups (8 animals per group) of control (without any treatment), TMT+PBS (Trimethyltin+Phosphate buffer saline), and TMT+Ad-MSC (Trimethyltin+Stem cells). For the induction of the AD, TMT was peritoneally injected (8 mg/Kg). After 48 h, the TMT+Ad-MSC group received 1 million stem cells intravenously. One month after transplantation, avoidance and working memories were evaluated. Afterward, hippocampal levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and malondialdehyde (MDA) were measured using ELISA.
Findings: The results showed a significant increase in the percentage of correct motor frequency in the Y maze, a decrease in the spent time in the dark room (P<0.05), and an increase in the latency time to the dark room in the TMT+Ad-MSC group, compared to the TMT+PBS group (P<0.01). Moreover, a significant increase in the CAT, SOD, and GPX enzymes activity, as well as a decrease in the MDA level in the hippocampus were observed in the TMT+Ad-MSC group, compared to the TMT+PBS group (P<0.05).
Discussion & Conclusion: Xenotransplantation of human adipose tissue stem cell improved learning and memory, reduced tissue oxidative stress, and increased hippocampal antioxidant capacity in an animal model of AD.

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Introduction: Many factors affect memory and learning. One of the most important ones is magnesium, which is essential for the proper functioning of our memory. Magnesium is the fourth most important cation and the second most important intracellular cation after potassium in the body. Magnesium plays an important role in neurotransmission. This study aimed to examine magnesium oxide nanoparticles' effect on the parameters of oxidative stress to treat memory deficit in the rat model of Alzheimer's disease with the help of Amyloid-β.
Material & Methods: In this experimental study, 54 adult male rats were divided randomly into nine groups, such as 1. Healthy control group, 2. Alzheimer's control group (rats that underwent stereotactic surgery and received 2nmol/µl of Amyloid-β by intracerebroventricular injection [ICVI]), 3. Sham group (rats that underwent stereotactic surgery and received saline as an Amyloid-β’s solvent), 4, 5, and 6. The healthy experimental groups (healthy rats receiving 2.5, 5, and 10 mg/kg body-weight doses of magnesium oxide nanoparticles by intraperitoneal injection), 7, 8, and 9. Alzheimer's experimental group (Alzheimer's rats receiving 2.5, 5, and 10 mg/kg body-weight doses of magnesium oxide nanoparticles by intraperitoneal injection). The duration of oral treatment of nanoparticles was 30 days. At the end of the treatment period (30 days), oxidative stress parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), and malondialdehyde (MDA) were measured in neural (brain tissue), and all data were analyzed by one-Factor ANOVA and Tukey post hoc test in SPSS software (version 21) considering a significance level of P<0.05.
(Ethic code: IR.IAU.SRB.REC.1398.126)
Findings: The results showed that magnesium oxide nanoparticles at 2.5, 5, and 10 mg/kg body-weight doses caused a significant reduction in malondialdehyde levels in Alzheimer's rats. Moreover, the number of antioxidant enzymes including GPX, SOD, and CAT in rats that received 2.5, 5, and 10 mg/kg body-weight doses of magnesium oxide nanoparticles increased significantly.
Discussion & Conclusion: The effect of oxidative stress on the progression of Alzheimer's disease and the antioxidant and inhibitor role of magnesium nano oxide in reducing the progression of this disease and on the neurophysiological brain functioning were confirmed. Furthermore, pathways involved in memory mechanisms are improved by mechanisms associated with Amyloid-β disorders.
 

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Introduction: Alzheimer's disease is a common progressive neurogenerative disease that leads to dementia and destruction of brain cells, especially in areas related to learning and memory such as the hippocampus. The role of the Arc gene in synaptic flexibility and memory consolidation has been proven and its expression is strongly influenced by neuronal activity. The aim of this study was to investigate the effect of Lactobacillus fermentum on the expression of Arc (effective in synaptic flexibility and memory consolidation) and CREB (effective in stabilizing synaptic changes during learning) genes, involved in the memory of Alzheimer's rats.
Material & ethods: In this study that was conducted in 2019, 30 male Wistar rats were divided into 5 groups (control, Alzheimer and 3 groups as treatment). In the treatment groups, simultaneously with induction of Alzheimer by stereotaxic method with streptozotocin, supernatant of Lactobacillus fermentum PTCC 1744 in MRS broth with doses of 10⁸, 10⁷, and 10⁶ cfu/ml was injected intraperitoneally for 21 days. After RNA extraction from hippocampus samples, cDNA was synthesized and the expression of the genes was evaluated by real-time PCR and LinReg PCR software.
Findings: The data showed an increase in gene expression of Arc and CREB in the treatment groups with a dose of 10⁶ cfu/ml compared to the Alzheimer's group and the difference was significant (P <0.001).
Discussion & conclusion: Extracellular compounds of L. fermentum may inhibit the progression of neuronal lesions due to their antioxidant and anti-inflammatory effects and may be effective in improving Alzheimer's.
 

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