Alzheimer’s disease (AD) is a severe neurological illness that causes memory loss and is a global problem. The calcium hypothesis recently steadily evolved in AD. The prospective targets for calcium homeostasis therapy, however, are limited, and gene expression-level research connected to calcium homeostasis in AD remains hazy. In this study, we analyzed the microarray dataset (GSE132903) taken from the Gene Expression Omnibus (GEO) database to investigate calcium homeostasis-related genes for AD. Using immunoblot analysis, we examined the association of ITPKB with inflammation in AD. Additionally, the immunofluorescence technique was employed to assess the impact of pharmacological inhibition of ITPKB on the amyloid-β (Aβ) plaque deposition in APP/PS1 mice. This article’s further exploration of calcium homeostasis-related genes has propelled the validation of the calcium homeostasis theory in AD.

阿尔茨海默病（AD）是一种严重的神经系统疾病，会导致记忆丧失，是一个全球性问题。钙假说最近在 AD 中稳步发展。然而，钙稳态治疗的预期目标是有限的，并且与 AD 中钙稳态相关的基因表达水平研究仍然模糊。在本研究中，我们分析了取自基因表达综合 (GEO) 数据库的微阵列数据集 (GSE132903)，以研究 AD 的钙稳态相关基因。使用免疫印迹分析，我们检查了 ITPKB 与 AD 炎症的关联。此外，采用免疫荧光技术评估 ITPKB 药理学抑制对 APP/PS1 小鼠中淀粉样蛋白-β (Aβ) 斑块沉积的影响。本文对钙稳态相关基因的进一步探索，推动了AD钙稳态理论的验证。