Introduction:  Amyloid beta (Aβ) is the major constituent of harmful plaques in the Alzheimer’s patients.  Thus, study of Aβ and understanding its related molecular and cellular mechanisms is essential for diagnosis and therapeutic interventions.  This study introduces a rapid, simple, and cost-effective technique for production and purification of this peptide, utilizing the expression of Aβ gene within bacterial system. Materials and methods: Aβ gene was synthesized and transferred into the expression vector pET26b. After induction by Lactose and  24 hours of incubation for Aβ expression the cell sediment was analyzed for presence of recombinant peptide using SDS-PAGE and Western blot.  Then the purification of recombinant peptide was carried using nickel chloride affinity chromatography. Characterization of purified Aβ was performed by evaluating cell cytotoxicity in 25 µM and 50 µM concentrations using MTT assay on Alzheimer cell line model SH-SY5Y. Results: Colony PCR and sequencing results showed the correct insertion of Aβ coding fragment into the expression vector. Presence of bands with the expected size in the results of SDS PAGE and western blot had confirmed successful expression of his-tagged recombinant peptide. MTT assay results showed the purified peptide has respectively 30 and 50% cytotoxicity for 25 µM and 50 µM concentrations. Discussion: Production of amyloid beta peptide in bacterial hosts seems to be favorable. Obtaining Aβ peptide in soluble phase is an important advantage of this study. Hence according to toxicity of the purified peptide, it can be utilized for cell line treatments and further researches on Alzheimer disease.

2Background: Oxidative stress and insulin resistance in type 2 diabetes are one of the factors in the development of cognitive disorders and Alzheimer's. So measuring the changes in beta amyloid gene expression and insulin resistance as one of the prominent disorders in type 2 diabetes, following HIIT and thyme’s honey consumption is the aim of the research. Methods: The present study was conducted with 36 young male Wistar rats, which were divided into 4 groups: control (C), interval training (T), thyme’s honey (H) and interval training-thyme’s honey (TH) was performed. The rats in the T and TH groups were trained for two months with intervals and intensity gradually increasing, and in the H and TH groups, they received 3 g/kg of thyme’s honey. Weight, fasting glucose and insulin were measured through the kit and insulin resistance index was done through the formula and gene expression were evaluated by RT-PCR. The findings were subjected to one-way and two-way ANOVA and Bonferroni's test. Results: Non-significant (NS) increase in weight, significant increase in insulin and significant decrease in gene expression in all intervention groups compared to C, significant decrease in fasting glucose in T and TH groups compared to C, significant decrease in insulin resistance in T group compared to other groups, NS increase was observed in group H and TH compared to C. Conclusion: HIIT and thyme’s honey had synergistic effect to reduce glucose and beta-amyloid gene expression as a preventive strategy for the occurrence of pathological features related to Alzheimer's and memory impairment in diabetics.

Dysregulation of brain cholesterol homeostasis causes the accumulation of extracellular protein deposits called amyloid plaques in the hippocampus which eventually leads to neuronal death, memory and learning deficits. The aim of the present study was to investigate the effect of beta amyloid on miRNAs regulating HMGCR and ABCA1 as cholesterol synthesis and homeostasis genes. Primary astrocytes were isolated from C57BL/6J mice, and were treated with 0. 5 μM amyloid beta (Aβ). Expression levels of genes and miRNAs were measured by real-time PCR. In comparison to control, Aβ treatment resulted in a significant decrease in miR-96-5p expression as a positive and negative regulator of HMGCR and ABCA1, respectively. There was no significant increase in miR-27a-3p expression as a negative regulator of HMGCR. miR-106b-5p and miR-143-3p expressions were also dramatically decreased as ABCA1 negative regulators. Amyloid beta can alter the expression of major genes in the cholesterol homeostasis pathway via their regulatory miRNAs.