Abstract
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.
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The key project of the Precision Medicine Joint Fund of the Natural Science Foundation of Hebei Province, Grant No. H2021206021, The 2022 Government-funded Provincial Medical Outstanding Talent Project.
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YH, FX, XR, and ML: methodology, data collection, and analysis, and manuscript preparation; ZZ and ZZ: study design and data interpretation. QW: manuscript revision. All authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.
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Hu, Y., Zhao, Z., Xu, F. et al. Transcriptome and Animal Model Integration Reveals Inhibition of Calcium Homeostasis-Associated Gene ITPKB Alleviates Amyloid Plaque Deposition. J Mol Neurosci 74, 42 (2024). https://doi.org/10.1007/s12031-024-02221-7
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DOI: https://doi.org/10.1007/s12031-024-02221-7