Abstract
Background: Although clinical vitamin A deficiency (VAD), which is a public health problem developing throughout the world, has been well controlled, marginal vitamin A deficiency (MVAD) is far more prevalent, especially among pregnant women and preschool children in China. Increasing evidence suggests that VAD is involved in the pathogenesis of Alzheimer’s disease (AD). However, whether MVAD, beginning early in life, increases the risk of developing AD has yet to be determined.
Objective: The goal of this study was to investigate the long-term effects of MVAD on the pathogenesis of AD in rats. Method: An MVAD model was generated from maternal MVAD rats and maintained with an MVAD diet after weaning. The males were bilaterally injected with aggregated amyloid β (Aβ)1–42 into the CA3 area of the hippocampus, and the AD-associated cognitive and neuropathological phenotypes were examined. Results: We found that MVAD feeding significantly aggravated Aβ1-42-induced learning and memory deficits in the Morris water maze test. MVAD did not induce the mRNA expression of retinoic acid receptors (RARs), a disintegrin and metalloprotease 10 (ADAM10) or insulin-degrading enzyme (IDE) in Aβ1-42-injected rats. Moreover, RARα and RARγ mRNA were positively correlated with ADAM10 mRNA, whereas RARβ mRNA was positively correlated with IDE mRNA. Conclusion: Our study suggests that MVAD beginning from the embryonic period perturbs the ADassociated genes, resulting in an enhanced risk of developing AD.Keywords: Alzheimer’s disease, amyloid β , vitamin A, marginal vitamin A deficiency, memory deficits, retinoic acid receptors, ADAM10, IDE.
Current Alzheimer Research
Title:Marginal Vitamin A Deficiency Exacerbates Memory Deficits Following Aβ1-42 Injection in Rats
Volume: 14 Issue: 5
Author(s): Jiaying Zeng, Tingyu Li, Ming Gong, Wei Jiang, Ting Yang, Jie Chen, Youxue Liu and Li Chen
Affiliation:
Keywords: Alzheimer’s disease, amyloid β , vitamin A, marginal vitamin A deficiency, memory deficits, retinoic acid receptors, ADAM10, IDE.
Abstract: Background: Although clinical vitamin A deficiency (VAD), which is a public health problem developing throughout the world, has been well controlled, marginal vitamin A deficiency (MVAD) is far more prevalent, especially among pregnant women and preschool children in China. Increasing evidence suggests that VAD is involved in the pathogenesis of Alzheimer’s disease (AD). However, whether MVAD, beginning early in life, increases the risk of developing AD has yet to be determined.
Objective: The goal of this study was to investigate the long-term effects of MVAD on the pathogenesis of AD in rats. Method: An MVAD model was generated from maternal MVAD rats and maintained with an MVAD diet after weaning. The males were bilaterally injected with aggregated amyloid β (Aβ)1–42 into the CA3 area of the hippocampus, and the AD-associated cognitive and neuropathological phenotypes were examined. Results: We found that MVAD feeding significantly aggravated Aβ1-42-induced learning and memory deficits in the Morris water maze test. MVAD did not induce the mRNA expression of retinoic acid receptors (RARs), a disintegrin and metalloprotease 10 (ADAM10) or insulin-degrading enzyme (IDE) in Aβ1-42-injected rats. Moreover, RARα and RARγ mRNA were positively correlated with ADAM10 mRNA, whereas RARβ mRNA was positively correlated with IDE mRNA. Conclusion: Our study suggests that MVAD beginning from the embryonic period perturbs the ADassociated genes, resulting in an enhanced risk of developing AD.Export Options
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Cite this article as:
Zeng Jiaying, Li Tingyu, Gong Ming, Jiang Wei, Yang Ting, Chen Jie, Liu Youxue and Chen Li, Marginal Vitamin A Deficiency Exacerbates Memory Deficits Following Aβ1-42 Injection in Rats, Current Alzheimer Research 2017; 14 (5) . https://dx.doi.org/10.2174/1567205013666161223162110
DOI https://dx.doi.org/10.2174/1567205013666161223162110 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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