Research: ZENG and COLLEAGUES,

Listed in Issue 251

Abstract

ZENG and COLLEAGUES, 1. Children's Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base for Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China; 2. Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China; 3. Townsend Family Laboratories, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada; 4. Children's Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base for Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. tyli@vip.sina.com; 5. Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. tyli@vip.sina.com;

6. Children's Nutrition Research Center, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base for Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. weihong@mail.ubc.ca ; 7. Chongqing Key Laboratory of Translational Medical Research in Cognitive Development and Learning and Memory Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. weihong@mail.ubc.ca ; 8. Townsend Family Laboratories, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada. weihong@mail.ubc.ca  researched the role of Vitamin A deficiency (VAD) and marginal vitamin A deficiency (MVAD) in the pathogenesis of Alzheimer’s disease (AD).

Background

Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the unique pathological hallmark of Alzheimer's disease (AD). Aβ is derived from amyloid β precursor protein (APP) by β- and γ-secretase cleavages and turned over by glia in the central nervous system (CNS).

Methodology

Vitamin A deficiency (VAD) has been shown to affect cognitive functions. Marginal vitamin A deficiency (MVAD) is a serious and widespread public health problem among pregnant women and children in developing countries. However, the role of MVAD in the pathogenesis of AD remains elusive.

Results

Our study showed that MVAD is approximately twofold more prevalent than VAD in the elderly, and increased cognitive decline is positively correlated with lower VA levels. We found that MVAD, mostly prenatal MVAD, promotes beta-site APP cleaving enzyme 1 (BACE1)-mediated Aβ production and neuritic plaque formation, and significantly exacerbates memory deficits in AD model mice. Supplementing a therapeutic dose of VA rescued the MVAD-induced memory deficits.

Conclusion

Taken together, our study demonstrates that MVAD facilitates AD pathogenesis and VA supplementation improves cognitive deficits. These results suggest that VA supplementation might be a potential approach for AD prevention and treatment.

References

Zeng J1,2,3, Chen L1,2, Wang Z3, Chen Q1,2, Fan Z1,2, Jiang H1,2, Wu Y3, Ren L1,2, Chen J1,2, Li T4,5, Song W6,7,8. Marginal vitamin A deficiency facilitates Alzheimer's pathogenesis. Acta Neuropathol: 133(6): 967-982. Jun  2017. doi: 10.1007/s00401-017-1669-y. Epub  Jan 27 2017.

Comment

The above research suggests that Vitamin A supplementation, by improving cognitive deficits might be a potential approach for Alzheimer's disease (AD) prevention and treatment.

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