A new Alzheimer's disease cell model using B cells to induce beta amyloid plaque formation and increase TNF alpha expression.

Different cell models have been developed for the study of Alzheimer's disease (AD) pathways. The neuronal dysfunction and cell death mechanisms that are commonly found in this disease are due to the production of high levels of cytokines and the formation of amyloid plaques. In the cell model introduced in the present study, the production of these two important factors is induced by using B cells from an AD patient. The B cells of an Alzheimer's patient and a normal control were immortalized by using EBV (Epstein-Barr virus) to produce a lymphoblastoid cell line (LCL). The amount of TNF alpha cytokine was evaluated at the RNA and protein levels by RT-PCR and ELISA, respectively. The AD LCL was cultured with SKNMC cells with and without treatment of TNF alpha siRNA. Amyloid plaque formation was monitored by Congo-red staining and microscopy. The amount of TNF alpha cytokine was significantly increased in the AD LCL compared to the normal LCL. The AD LCL induced the formation of amyloid plaques in SKNMC cells. The AD LCL treated with TNF alpha siRNA and co-cultured with SKNMC cells decreased the size and number of amyloid plaques in SKNMC cells. This cellular model is an appropriate model for studying Alzheimer's disease and the mechanisms related to it, as well as for research on cytokine inhibitors, especially TNF alpha inhibitors.