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PO1-1-26

Exploring the therapeutic potential of vitamin D supplementation for Alzheimer's disease

[Speaker] Fang-Yu Lin:1
[Co-author] Hsiao-Wei Jao:2, Ya-Hsin Hsiao:1
1:Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan, 2:School of Pharmacy, College of Medicine, National Cheng-Kung University, Tainan, Taiwan

Alzheimer's disease (AD) is the most common form of dementia, affecting up to 70% of all people with dementia. The most common early symptom of AD is difficult to remember newly learned information. The classical functions of vitamin D are known to play an essential role in calcium and phosphate homeostasis and in bone health. In addition, recent studies suggest that vitamin D is also implicated in cognitive and neuroprotective functions. Epidemiological and clinical data show that high serum levels of vitamin D link with better cognitive test performance, whereas increasing evidence suggests the concentrations of vitamin D would be associated with AD. In addition, the consequences of vitamin D deficiency are severe and can be observed in many diseases progression, especially AD. Emerging evidence reveals that low serum vitamin D concentrations are associated with a substantially increased risk of all-cause dementia and Alzheimer disease. However, the potential beneficial therapeutic strategy of vitamin D supplementation against AD still need to be further delineated. Therefore, we hypothesized that vitamin D supplementation may have therapeutic efficacy to slow down the AD progression in this study. In order to achieve the purpose, we utilized triple transgenic mice (3xTg-AD) as an AD mouse model. We found that vitamin D concentrations were significantly lower in 3xTg-AD mice, compared to control mice. In addition, vitamin D supplementation improved cognitive deficits in 3xTg-AD mice, using object location and water maze tests. This study would make a valuable contribution to the development of promising strategies for management, prevention, and treatment of AD.
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