title: Vitamin D3-enriched diet correlates with a decrease of amyloid plaques in the brain of AβPP transgenic mice.
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.
authors.affiliation: Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Jin
authors.initials: J
authors.lastname: Yu
authors.forename: Marco
authors.initials: M
authors.lastname: Gattoni-Celli
authors.forename: Hong
authors.initials: H
authors.lastname: Zhu
authors.forename: Narayan R
authors.initials: NR
authors.lastname: Bhat
authors.forename: Kumar
authors.initials: K
authors.lastname: Sambamurti
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Gattoni-Celli
authors.forename: Mark S
authors.initials: MS
authors.lastname: Kindy
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001842:Bone and Bones / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D002762:Cholecalciferol / Q000008:administration & dosage* / Q000097:blood; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D006801:Humans; D007859:Learning Disabilities / Q000178:diet therapy / Q000209:etiology; D008297:Male; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D008569:Memory Disorders / Q000178:diet therapy / Q000209:etiology; D051379:Mice; D008822:Mice, Transgenic; D051839:NFI Transcription Factors / Q000378:metabolism; D020932:Nerve Growth Factor / Q000378:metabolism; D058225:Plaque, Amyloid / Q000178:diet therapy* / Q000235:genetics / Q000473:pathology*; D053764:Presenilin-1 / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016564:Amyloid beta-Protein Precursor; C077305:CTF-1 transcription factor; D051839:NFI Transcription Factors; C508853:PSEN1 protein, human; D053764:Presenilin-1; D014409:Tumor Necrosis Factor-alpha; D002762:Cholecalciferol; D020932:Nerve Growth Factor