CK2-dependent SK channel dysfunction as contributor to neuronal hyperexcitability in Alzheimer's disease

Xiaojie Wei; Binggui Sun

doi:10.1016/j.tins.2024.12.006

CK2-dependent SK channel dysfunction as contributor to neuronal hyperexcitability in Alzheimer's disease

Trends Neurosci. 2025 Jan 4:S0166-2236(24)00250-9. doi: 10.1016/j.tins.2024.12.006. Online ahead of print.

Authors

Xiaojie Wei¹, Binggui Sun²

Affiliations

¹ Department of Anesthesiology of the Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine and National Clinical Research Center for Child Health, Zhejiang University, Hangzhou, Zhejiang Province 310058, China; Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province 310020, China.
² Department of Anesthesiology of the Children's Hospital and School of Brain Science and Brain Medicine, Zhejiang University School of Medicine and National Clinical Research Center for Child Health, Zhejiang University, Hangzhou, Zhejiang Province 310058, China; NHC and CAMS Key Laboratory of Medical Neurobiology, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, Zhejiang Province 310058, China. Electronic address: bsun@zju.edu.cn.

PMID: 39757072
DOI: 10.1016/j.tins.2024.12.006

Abstract

Neuronal hyperexcitability in the cortex and hippocampus represents an early event in Alzheimer's disease (AD). In a recent study, Blankenship and colleagues reported that in a mouse of AD, ventral tegmental area (VTA) dopamine neurons are also hyperexcitable, and this hyperexcitability is due to casein kinase 2 (CK2)-dependent SK channel dysfunction, adding new insights into the underlying mechanisms of aberrant neuronal properties in AD.

Keywords: circuit pathology; dopamine neuron; ion channel; memory; neurodegeneration; ventral tegmental area.