Affiliations: [a] Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA | [b] Department of Radiation Oncology, Medical University of South Carolina, Charleston, SC, USA | [c] Ralph H. Johnson VA Medical Center, Charleston, SC, USA
Correspondence:
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Correspondence to: Mark S. Kindy, Ph.D., Department of Neurosciences, Strom Thurmond Biomedical Research Building, Room 503, 114 Doughty Street, Charleston, SC 29403, USA. Tel.: +1 843 792 0808; Fax: +1 843 876-5099; E-mail: kindyms@musc.edu.
Abstract: In addition to its function in calcium and bone metabolism, vitamin D is neuroprotective and important for mitigating inflammation. Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the central nervous system, characterized by neuronal loss in many areas of the brain, and the formation of senile (neuritic) plaques, which increase in number and size over time. The goal of this project was to investigate whether vitamin D3 supplementation would affect amyloid plaque formation in amyloid-β protein precursor (AβPP) transgenic mice that spontaneously develop amyloid plaques within 3–4 months of birth. AβPP mice were fed control, vitamin D3-deficient or vitamin D3-enriched diets for five months, starting immediately after weaning. At the end of the study, the animals were subjected to behavioral studies, sacrificed, and examined for bone changes and brain amyloid load, amyloid-β (Aβ) peptide levels, inflammatory changes, and nerve growth factor (NGF) content. The results obtained indicate that a vitamin D3-enriched diet correlates with a decrease in the number of amyloid plaques, a decrease in Aβ peptides, a decrease in inflammation, and an increase in NGF in the brains of AβPP mice. These observations suggest that a vitamin D3-enriched diet may benefit AD patients.
Keywords: Alzheimer's disease, amyloid-β, animal models, transgenic mice, vitamin D
