4.7 Article

High-dose of vitamin C supplementation reduces amyloid plaque burden and ameliorates pathological changes in the brain of 5XFAD mice

期刊

CELL DEATH & DISEASE
卷 5, 期 -, 页码 -

出版社

NATURE PUBLISHING GROUP
DOI: 10.1038/cddis.2014.26

关键词

Alzheimer's disease; 5XFAD mice; Vitamin C; amyloid plaque; BBB disruption; mitochondrial dysfunction

资金

  1. National Research Foundation [2009-0080348, 2012R1A2A1A01002881]
  2. Medical Research Center [2011-0030738]
  3. KRIBB Research Initiative Program
  4. KIST Institutional Program [2E24242-13-135]
  5. Korea National Institute of Health ROAD R&D Program Project [A092058]
  6. Korea Health Promotion Institute [A092058] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  7. National Research Foundation of Korea [2009-0080348] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Blood-brain barrier (BBB) breakdown and mitochondrial dysfunction have been implicated in the pathogenesis of Alzheimer's disease (AD), a neurodegenerative disease characterized by cognitive deficits and neuronal loss. Besides vitamin C being as one of the important antioxidants, recently, it has also been reported as a modulator of BBB integrity and mitochondria morphology. Plasma levels of vitamin C are decreased in AD patients, which can affect disease progression. However, investigation using animal models on the role of vitamin C in the AD pathogenesis has been hampered because rodents produce with no dependence on external supply. Therefore, to identify the pathogenic importance of vitamin C in an AD mouse model, we crossbred 5 familial Alzheimer's disease mutation (5XFAD) mice (AD mouse model) with i-gulono-c-lactone oxidase (Gulo) knockout (KO) mice, which are unable to synthesize their own vitamin C, and produced Gulo KO mice with 5XFAD mice background (KO-Tg). These mice were maintained on either low (0.66 g/l) or high (3.3 g/l) supplementation of vitamin C. We found that the higher supplementation of vitamin C had reduced amyloid plaque burden in the cortex and hippocampus in KO-Tg mice, resulting in amelioration of BBB disruption and mitochondrial alteration. These results suggest that intake of a larger amount of vitamin C could be protective against AD-like pathologies.

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