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Alzheimer's disease (AD) is a common cause of dementia in elderly people that is accompanied by progressive cognitive decline and memory loss. The pathologic hallmarks of AD are synaptic and neuronal degeneration together with extracellular senile plaques containing amyloid-beta (Aβ) and the intracellular neurofibrillary tangles (NFTs) in the hippocampus and other cortical regions. Amyloid-beta peptide is believed to have a pivotal role in the pathogenesis of AD as a major component of the senile plaques. It acts as a trigger key of AD and is considered as the principal toxic factor in the pathogenesis of the disease. Accumulation of amyloid β protein (Aβ), a main component of the senile plaques, in the brain initiates a cascade of events that ultimately lead to neuronal dysfunction and cognitive deficits. Other proposed mechanisms for AD include impairment in cholinergic function, oxidative stress, inflammatory agents and glutamate-mediated excitotoxicity. AD is characterized neuropathologically by impaired cholinergic function, increased oxidative stress, neuroinflammation, neuronal cell death, synapses loss, cortical atrophy, deficiencies in steroid hormones and appearance of glutamate-mediated excitotoxicity.

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Background & objectives: Exercise, with beneficial effects on brain health and cognitive function reduces the destructive effects of some neurological diseases such as Alzheimer's. The aim of this study was to evaluate the effect of four weeks of aerobic exercise on cognitive function and expression of Sirt1, CREB and BDNF genes in the hippocampus of male Wistar rats with Alzheimer's disease.
Methods: The statistical population included 18 male Wistar rats from the Pasteur Institute. Rats were randomly divided into three groups including Alzheimer's group, Alzheimer's disease-exercise group and a healthy control group. Alzheimer's disease group was induced by injecting Aβ42 into the hippocampus. Seven days after surgery, the rats performed the aerobic exercise for four weeks (five sessions per week at a speed of 10-15 m/min). They underwent behavioral tests 48 hours after the last training session. Twenty four hours later, rat hippocampal tissue was extracted. Sirt1, CREB and BDNF mRNAs were measured using Real time-PCR.
Results: Learning and spatial memory performance decreased in rats of Alzheimer's disease group compared to a healthy control group (p˂0.001). Decreased mRNA expression of Sirt1, CREB and BDNF genes was observed in the hippocampal tissue of Alzheimer's disease group compared with the healthy control group (p˂0.001). Alzheimer's rats with intermittent aerobic exercise had improved learning function, spatial memory and increased mRNA expression levels of Sirt1, CREB and BDNF genes in comparison with Alzheimer's disease group (p˂0.001).
Conclusions: Periodic aerobic exercise in rats with Alzheimer's disease can improve spatial learning and memory by positively regulating the Sirt1/ CREB/ BDNF signaling pathway in hippocampal tissue.

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Background & objectives: Alzheimer’s disease (AD) patients suffer from anxiety and depression. Sodium hydrosulfide (NaHS) can remit the depressive-like and anxiety-like behaviors induced by diabetes mellitus. We aimed to investigate the effects of chronic administration of hydrogen sulfide on depressive and anxiety-like behaviors in the Streptozotocin (STZ) rat model of AD.
Methods: Animals were divided into: Control, NaHS, and Alzheimer’s rats group include (STZ, STZ + Saline and STZ + NaHS groups) which were the Alzheimer’s rats and received Saline and NaHS (5.6 mg/kg per d) for 21 days. For induction of AD, STZ (3 mg/kg, 10 μl/injection site) was administered into the lateral ventricles. The behavioral consequences were assessed using plus maze, forced swim and sucrose preference tests.
Results: Our results showed that intracerebroventricular (i.c.v.) injection of STZ decreased the percentage of open arm time and entries, indicating anxiety-like effects. It also increased the duration of immobility time and decreased the percentage of sucrose preference indicating depression-like effects. Sodium hydrosulfide administration in STZ-treated rats increased the percentage of open arm time and entries, indicating anxiolytic-like effects. It also decreased the duration of immobility time and increased the percentage of sucrose preference, indicating antidepressant-like effects.
Conclusion: STZ administration can induce depression- and anxiety-like symptoms in rats, and Sodium hydrosulfide treatment, decreased the depression- and anxiety-like symptoms in STZ rat Model of AD, suggests that Sodium hydrosulfide can be useful in the treatment of affective disorders in AD patients.

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Background & objective: Alzheimer's disease (AD) is the most common cause of dementia among the elderly, threatening their quality of life. On the other hand, regular exercise is associated with improved brain health and cognitive function. However, the mechanisms of these benefits have not yet been fully elucidated. Therefore, the aim of this study was to investigate the effect of 4 weeks of moderate intensity interval aerobic training on cognitive function and expression level of PGC1α and VEGF genes in the hippocampus of old rats with AD.
Methods: For this purpose, 20-month-old male Wistar rats were divided into three groups of AD (n=8), AD+exercise training (n=8) and control (n=8). Intra-hippocampal injection of Aβ₄₂ was used to induce AD. The animals in the exercise group performed moderate-intensity interval aerobic exercise for 4 weeks, 5 days a week. To assess spatial learning and memory, the animals underwent the Morris water maze test 48 hours following the last training session. Then, the animals were killed and hippocampal tissue was extracted. Real time-PCR method was used to measure gene expression. Statistical analysis was performed using one-way analysis of variance and Pearson correlation coefficient at the significance level of p£0.05.
Results: The results showed that Aβ₄₂ injection impaired spatial learning and memory function and reduced the expression level of PGC1α and VEGF genes in hippocampal tissue (p£0.05). Aerobic exercise improved spatial learning and memory function and increased PGC1α and VEGF genes expression (p£0.01). Also, a significant positive relationship was observed between the PGC1α and VEGF gene expression levels in the hippocampus (r= 0.859, p≤0.01). In addition, there was a significant inverse relationship between PGC1α and VEGF genes expression and the mean time spent to find the platform (r= -0.9, p£0.01 and r= -0.750, p£0.01, respectively), and a significant positive relationship with the time spent in the target quadrant (r= -0.794, p£0.01 and r= -0.632, p£0.01, respectively).
Conclusion: In general, aerobic training improves spatial learning and memory performance in old animals with AD; up-regulation of the exercise-induced PGC1α/VEGF pathway in the brain, at least in part, appears to be involved in this adaptation.

 

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Background & objectives: There is a tendency to increase the risk of dementia in patients with periodontitis, but the opposite, the role of Alzheimer's disease on periodontal disease is still unclear, so in this study, the effect of experimental Alzheimer's disease on periodontal inflammatory cells, collagen fibers and neovascularization was investigated in male rats.
Methods: In this experimental study, 16 Wistar male rats (230-250 grams) were randomly divided into 2 groups; control (saline) and streptozotocin 3 mg/kg (bilateral ICV injection, with a volume of 10 μl, in both groups). After 4 weeks of treatment, two groups were tested with the Morris water maze. Then the rats were killed by deep anesthesia and sampling from the papilla around the two central incisor teeth was done. Samples were fixed and the paraffin block was prepared, serial 5-micron slices were made with a microtome. After hematoxylin & eosin staining, the number of inflammatory cells (PMNs, eosinophils, and mast cells), angiogenesis, and fibroblasts were counted using a microscope (400×). Data were analyzed using SPSS 21 software and an independent T-test.
Results: The results showed that Alzheimer's disease causes an increase in periodontal inflammatory cells, collagen fibers and new vessels in the gums of mice, and the difference between these changes between the experimental and control groups was significant in all parameters (p<0.00).
Conclusion: According to these findings, Alzheimer's disease causes or aggravates inflammation and increases the rate of periodontal diseases in rat and may have the same effect in humans.
 

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Background & objective: The causes of Alzheimer's disease are currently unknown. Genetic and environmental factors can be effective in creating of this disease. In recent studies, one of the genes and its polymorphisms that was known to affect Alzheimer is SHARPIN. This study aimed to investigate the presence of rs34674752 polymorphism in the SHARPIN gene and its relation with Alzheimer's disease in the population of Iranian patients.
Methods: This study was performed on 50 people with Alzheimer's disease and 50 healthy controls. After blood sampling and DNA extraction, genotyping was done by Tetra ARMS PCR. The data was statistically analyzed.
Results: Results showed that the frequency of GG, GT and TT genotypes of rs34674752 polymorphism in control and patient groups was 100%, 0% and 0%, respectively. Both control and patient groups were in Hardy Weinberg equilibrium. There was no significant correlation between people's genotype and the possibility of Alzheimer's disease, and among the demographic factors, only the relationship between age group and the disease was significant (p=0.029).
Conclusion: According to the results of this study, there was no statistically significant association between the rs34674752 polymorphism in the SHARPIN gene and Alzheimer's disease in the studied Iranian population. To confirm the present study results, the investigation of populations with different societies and a larger quantity of samples are recommended.