alexa Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis
ISSN: 0974-8369

Biology and Medicine
Open Access

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Research Article

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Vanessa Cavalcante da Silva1, Leandro Fernandes1, Ana Luiza Dias Abdo Agamme1, Eduardo Jun Haseyama1, Maria Tereza Cartaxo Muniz2 and Vânia D’Almeida1*

1Department of Psychobiology, Universidade Federal de São Paulo, R. Sena Madureira, 1500 - Vila Clementino, São Paulo, Brazil

2Pediatrics Hematology and Oncology Center, Biological Science Institute, Universidade de Pernambuco, Recife, Pernambuco, Brazil

*Corresponding Author:
Vânia D’Almeida
Department of Psychobiology
Universidade Federal de São Paulo
R. Sena Madureira, 1500 - Vila Clementino
São Paulo - SP, 04021-001, Brazil
Tel: 55-11-21490155 ext. 283
Fax: 55-11-55725092
E-mail: [email protected]

Received Date: February 01, 2017; Accepted Date: March 03, 2017; Published Date: March 10, 2017

Citation: da Silva VC, Fernandes L, Agamme ALDA, Haseyama EJ, Muniz MTC, et al. (2017) Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’s Disease Pathogenesis. Biol Med (Aligarh) 9: 393. doi:10.4172/0974-8369.1000393

Copyright: © 2017 da Silva VC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Alzheimer's disease (AD) is characterized by progressive neurodegenerative impairment of the central nervous system and is the most prevalent form of dementia. Considering the influence of maternal nutrition on fetal programming, which consequences usually come later in life, we investigated whether maternal vitamin B deficiency during early development alters the offspring expression of genes related to AD etiopathogenesis. Mice dams were submitted to experimental diet one month before and during pregnancy or pregnancy/lactation and, after birth, their offspring were distributed into three groups: control “CT”, deficient pregnancy “DP” and deficient pregnancy and lactation “DPL”. At postnatal day (PND) 0, a significant decrease of App in females (p=0.007) and App and Bace1 in males (p=0.030 and p=0.040, respectively) was observed when compared to CT group. At PND 28, DPL female presented an increase of App, Bace1 and Ps1 gene expression when compared to CT (p=0.003, p=0.003 and p=0.002, respectively) and DP groups (p=0.017, p=0.005 and p=0.002, respectively). In males at PND 28, a decrease of App and Ps1 was observed in both DP (p=0.012; p=0.001) and DPL (p=0.001; p=0.04) when compared to CT group. No differences were observed in females and males at PND 210. Regarding APP, BACE1 and PS1 protein expression and global DNA methylation pattern, no difference was observed throughout development in female or male offspring. Regarding behavioral evaluations, no changes were observed in the object recognition task, but the DPL males presented lower locomotor activity when compared to DP (p=0.028) and CT (p=0.003) groups. In conclusion, the early exposition to vitamin B deficiency alters the expression of genes related to AD.

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