Effects of Specific Inhibitors for CaMK1D on a Primary Neuron Model for Alzheimer’s Disease

Molecules

Satyabrata Kar¹  Paige Grant²  Jitendra Kumar²  Michael Overduin² 

[1] Centre for Prions and Protein Folding Diseases, Department of Medicine (Neurology), University of Alberta, Edmonton, AB T6G 2MB, Canada;Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada;

关键词: Alzheimer’s disease;    kinase inhibitor;    CaMK1D;    beta-amyloid;    tau phosphorylation;   

DOI  :  10.3390/molecules26247669

来源: DOAJ

【 摘 要 】

Alzheimer’s disease (AD) is the most common cause of dementia worldwide. Despite extensive research and targeting of the main molecular components of the disease, beta-amyloid (Aβ) and tau, there are currently no treatments that alter the progression of the disease. Here, we examine the effects of two specific kinase inhibitors for calcium/calmodulin-dependent protein kinase type 1D (CaMK1D) on Aβ-mediated toxicity, using mouse primary cortical neurons. Tau hyperphosphorylation and cell death were used as AD indicators. These specific inhibitors were found to prevent Aβ induced tau hyperphosphorylation in culture, but were not able to protect cells from Aβ induced toxicity. While inhibitors were able to alter AD pathology in cell culture, they were insufficient to prevent cell death. With further research and development, these inhibitors could contribute to a multi-drug strategy to combat AD.

【 授权许可】

Unknown