AI Article Synopsis
- Vitamin D supplementation may offer a new treatment avenue for Alzheimer's disease, but its mechanisms are not fully understood.
- The cytokine IL-34 plays a role in protecting neurons and is up-regulated by the active form of vitamin D, 1α,25-dihydroxyvitamin D3, in neuronal cells.
- This study indicates that 1α,25(OH)D induces IL-34 expression via the vitamin D receptor, potentially explaining how vitamin D protects against Alzheimer's disease.
Article Abstract
Vitamin D supplementation is regarded as a novel approach to treat Alzheimer's disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)D]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α,25(OH)D through the vitamin D receptor (VDR). Furthermore, we identified the core promoter of IL-34 gene and a VDR binding site (CGCCCT) that was required for 1α,25(OH)D-induced IL-34 expression. These findings suggest that the induction of IL-34 expression by 1α,25(OH)D may constitute a mechanism that explains the protective function of vitamin D in Alzheimer's disease.
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| http://dx.doi.org/10.1177/1753425917725391 | DOI Listing |
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