Hyperexpression of STIM2 protein lowers the amount of Abeta plaques in the brain of Alzheimer's disease mouse model

Abstract

The role of the STIM2→nSOCE signaling pathway was investigated in a model of Alzheimer's disease (AD) 5FAD mice that express amyloid and presenilin toxicity simultaneously. It was observed that expression of STIM2 protein was downregulated in the hippocampus of adult 5FAD mice at the age of 4 and 6 months. It was shown that expression of PSD95 protein was downregulated together with STIM2 protein. It was established that hyperexpression of STIM2 protein in the hippocampus of adult mice lowered the amount of amyloid plaques in the cortex of 5FAD mice by three times. The observed data confirms the scientific hypothesis that activation of STIM2-dependent store-operated calcium entry can have a therapeutic effect for treatment in AD.