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Alzheimer's disease (AD) is a neurodegenerative disorder, which has become the leading cause of dementia cases globally. Synaptic failure is an early pathological feature of AD. However, the cause of synaptic failure in AD, especially the GABAergic synaptic activity remains unclear. Extensive evidence indicates that the presence of soluble amyloid-β is an early pathological feature in AD, which triggers synaptic dysfunction and cognitive decline. Our recent study explored the relation of GABAergic transmission and soluble Aβ in early APP/PS1 mice. Firstly, we found soluble Aβ42 levels were significantly increased in serum, hippocampus and prefrontal cortex in 3-4 months APP/PS1 mice, which was much earlier than Aβ plagues formation. In addition, we found TNF-α and BDNF expression levels were increased, while KCC2 and GABA A R expression were decreased in 3-4 months APP/PS1 hippocampus. When we treated 3-4 months APP/PS1 mice with a potent γ-secretase inhibitor, LY411575, which can reduce the soluble Aβ42 levels, the TNF-α and BDNF protein levels were decreased, while KCC2 and GABA A R levels were increased. In conclusion, our study suggested soluble Aβ may impaired the GABA inhibition by mediating KCC2 levels in early APP/PS1 mice. KCC2 may be served as a potential biomarker for AD.

Soluble β-amyloid impaired the GABA inhibition by mediating KCC2 in early APP/PS1 mice