ASSESSING THE ROLE OF EBV PROTEINS IN AMYLOID-BETA AGGREGATION ASSOCIATED WITH INDUCTION OF ALZHEIMER'S DISEASE

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dc.contributor.authorBerikkara, Assel
dc.date.accessioned2024-05-14T11:55:01Z
dc.date.available2024-05-14T11:55:01Z
dc.date.issued2024-04-26
dc.description.abstractBackground: Alzheimer’s disease represents the most prevalent form of neurocognitive decline. The key distinguishing pathological markers within the central nervous system involve the aggregation of senile plaques resulting from a two-step cleavage of the amyloid precursor protein by beta- and gamma-secretase enzymes sequentially. Previous studies have demonstrated a positive correlation between individuals who have mononucleosis due to EBV infection and their increased vulnerability to Alzheimer's disease. Hence, a new outlook on the disease etiology known as the "infectious hypothesis" has directed attention toward the Epstein-Barr virus (EBV), a double-stranded DNA virus, in terms of its potential contribution to plaque formation and inflammation associated with Alzheimer's disease. Methods: H4 neuroglioma and U118 glioblastoma cell lines were directly infected with EBV containing supernatant. The expression of APP and Tau mRNA was detected by qPCR. Protein levels were measured using ELISA with anti-APP antibodies, both before and after viral infection. Virus-free H4 and U118 cell lines were used as controls for comparative statistical analysis of mRNA and protein levels of the APP gene. Results: Infected U118 cell growth was maintained for more than 20 days, while H4 cells died out after the 7th day post-infection. qPCR results showed a consistent decrease in wild-type APP, APP-KPI, and APP-770 mRNA levels throughout the infection period, while Tau protein exhibited a statistically significant decrease in its expression level. In H4 cells, there was a decrease in WT APP and APP-KPI, while tau protein showed an enhanced mRNA level compared to the control. Conclusion: Direct EBV infection of glial cells resulted in alterations in the expression of Alzheimer's disease hallmark genes (WT APP, APP-770, APP-751, and Tau) in both H4 and U118 cell lines in a time-dependent manner.en_US
dc.identifier.citationBerikkara, Assel (2024). Assessing the role of EBV proteins in amyloid-beta aggregation associated with induction of Alzheimer's disease, Nazarbayev University School of Medicineen_US
dc.identifier.urihttp://nur.nu.edu.kz/handle/123456789/7663
dc.language.isoenen_US
dc.publisherNazarbayev University School of Medicineen_US
dc.subjectAlzheimer’s Diseaseen_US
dc.subjectEBV infectionen_US
dc.subjectinfectious hypothesisen_US
dc.subjectamyloid precursor proteinen_US
dc.subjectbeta-amyloiden_US
dc.subjecttau proteinsen_US
dc.subjectH4en_US
dc.subjectU118 cell linesen_US
dc.titleASSESSING THE ROLE OF EBV PROTEINS IN AMYLOID-BETA AGGREGATION ASSOCIATED WITH INDUCTION OF ALZHEIMER'S DISEASEen_US
dc.typeMaster's thesisen_US
workflow.import.sourcescience

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