Na⁺‐Ca²⁺ exchanger isoform‐3 in Aβ_1‐42‐induced Alzheimer’s disease pathology

Abstract Background The relevance of a plasma membrane Na + ‐Ca 2+ exchanger isoform‐3 protein, NCX3, is widely evidenced in neuronal physiology. However, the mechanisms leading to NCX3 expression deficits in Alzheimer’s disease (AD) pathology and its value as a target in AD pharmacological medicine remain incomplete. Methods Inhibition and rescue experiments were performed in cultured primary neurons of 5×FAD mice model of AD using pathological Aβ 1‐42 isolated from a conditioned medium of BHK cells, a cell line which does not constitutively express NCX3, stably transfected with a plasmid expressing human wild type Aβ 1‐42 . Results Pathological forms of Aβ 1‐42 interfere with NCX3 expression level and neuronal viability. Pronounced expression levels of NCX3 and state of endurance were observed in the control group compared with those treated with pathological Aβ 1‐42 . Conclusion NCX3 merits in‐depth study consideration as a predictive biomarker and in developing a potential novel pharmaceutical intervention method for AD. Keywords : Alzheimer’s disease, Aβ 1‐42 , Na + ‐Ca 2+ exchanger isoform‐3