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Background and Objectives: Alzheimer’s disease is the most common neurodegenerative disease and the memory impairment is the main prominent symptom of this disease. The hippocampus of the brain, is the first region that undergoes changes in Alzheimer’s. Systems biology tools such as high-throughput techniques, enable us to explore signature genes involved in disease initiation and advancement which can be considered as new therapeutic and diagnostic candidates in complex diseases like Alzheimer’s.
Methods: A total of 85 samples obtained from the hippocampus of the brain of healthy individuals and individuals with Alzheimer’s were selected from two datasets. Differential expression analysis was performed independently for both datasets and the results were integrated. Genes with the same expression pattern in the two datasets were used to construct a gene-gene network using the STRING database. The obtained network analysis was performed to detect key genes associated with the disease.
Results: In this study, 73 genes with the same expression pattern were found in the two datasets. The obtained network analysis led to the identification of SNAP25, UNC13A, SYN2 and AMPH as key genes connected with Alzheimer’s disease.
Conclusion: The role of the reported key genes in endocytosis, neurotransmitters release and synaptic vesicle cycle facilitate proper functioning of memory. Expressional changes and mutations in each of these genes effect other pathways and lead to Alzheimer’s. Thus, the key genes reported in this study, can be considered as potential markers in developing diagnostic and therapeutic methods for Alzheimer’s.

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Objective: Low density Lipo-protein Receptor- related Protein (LRP) is the most important cholesterol receptor in neurons. It serves as a receptor for APOE protein which is the most important risk factor for Alzheimer’s Disease. LRP also contributes to the ligation of lipoproteins with APOE in neurons. Association between LRP C766T and Alzheimer’s disease in Iranian patients with late onset Alzheimer’s disease (LOAD) was investigated in this research. Materials and Methods: 100 patients with LOAD were selected based on DSM-IV-TR and NINCDS-ADRDA diagnostic criteria and 100 normal controls without any personal and family history of Alzheimer’s disease or dementia were included in this case- control study. AD patients and control subjects were matched for age and sex. PCR-RFLP was set up to detect LRP C766T polymorphism. Results: LRP C/C genotype and C allele distribution were more frequent in AD patients than in control subjects. However, this difference was not statistically significant. When association between LRP C/C genotype and AD was categorized by the gender, in both genders, there was not any significant correlation. Conclusion: Our findings indicate that 766C allele of LRP gene could not significantly alter the risk of developing late-onset Alzheimer's disease in Iranian patients. Analysis of other genetic factors and environmental factors are promoted in Iranian population.

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Alzheimer’s disease (AD) is the most common type of dementia in the elderly. The neuropathology and treatment of AD is not precisely determined yet, but according to the pathological studies, AD is associated with presence of toxic soluble oligomers and insoluble senile plaques formed by amyloidosis of Amyloid Beta (Aβ) in neocortical region of brain. The V10HHQKLVFFAE22 is a critical region of Aβ42 which facilitates aggregation process. An attractive therapeutic approach to treat AD is to identify small ligands that are capable of binding to critical residues in order to inhibit or reverse Aβ amyloidosis process as source of neurotoxicity. In this area, therapeutic efforts designed various organic agents and most of them focused on the N-terminal sequence of Aβ. Here, a peptide inhibitor derived from the C-terminal of Aβ (G33LMVG37) is utilized as inhibitor and combined Docking and Molecular dynamics simulation used to find the binding sights in the critical region (V10HHQKLVFFAE22). The simulation identified tree stable binding sites for Aβ42 inhibition by penta peptide. This result indicate that this penta-peptide is capable to inhibit aggregation process and can be consider as an drug for AD preclinical studies.