Maternal imprinting on cognition markers of wild type and transgenic Alzheimer's disease model mice.

Data de publicació: 24/04/2018

Autors de IIS La Fe

Juan Sandoval Del Amor

Autor

Autors aliens a IIS La Fe

Zamarbide, M
Gil-Bea, FJ
Bannenberg, P
Martinez-Pinilla, E
Franco, R
Perez-Mediavilla, A

Grups d'Investigació

Unidad de Biomarcadores y Medicina de Precisión (UBYMP)

Leader

Agustín Lahoz Rodríguez

Abstract

The risk of suffering from Alzheimer's disease (AD) is higher in individuals from AD-affected mothers. The purpose of this investigation was to study whether maternal transmission might produce AD-related alterations in progenies of mice that do not have any genotypic alteration. We used cognitively-intact mothers harbouring in heterozygosity the transgene for overexpressing the Swedish double mutant version of the human amyloid precursor protein (hAßPPswe). The phenotype of the offspring with or without the transgene resulting from crossing young Tg2576 females with wild-type males were compared with those of the offspring resulting from crossing wild-type females with Tg2576 males. The hAßPPswe-bearing offspring from Tg2576 mothers showed an aggravated AD-like phenotype. Remarkably, cognitive, immunohistochemical and some biochemical features displayed by Tg2576 heterozygous mice were also found in wild-type animals generated from Tg2576 females. This suggests the existence of a maternal imprinting in the wild-type offspring that confers a greater facility to launch an AD-like neurodegenerative cascade. Such progeny, lacking any mutant amyloid precursor protein, constitutes a novel model to study maternal transmission of AD and, even more important, to discover early risk markers that predispose to the development of AD.

Dades de la publicació

ISSN/ISSNe:: 2045-2322, 2045-2322
Tipus:: Article
Pàgines:: 6434-6434
DOI:: 10.1038/s41598-018-24710-7
PubMed:: 29691440
Factor d'Impacte:: 1,414 SCImago ℠
Quartil:: Q1 SCImago ℠

Documents

No hi ha documents

Mètriques

Filiacions

Zamarbide, M:: Neuroscience Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain.

Univ Navarra, Ctr Appl Med Res CIMA, Neurosci Dept, Pamplona, Spain
Gil-Bea, FJ:: Neuroscience Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain

Univ Navarra, Ctr Appl Med Res CIMA, Neurosci Dept, Pamplona, Spain
Bannenberg, P:: Neuroscience Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain

Univ Navarra, Ctr Appl Med Res CIMA, Neurosci Dept, Pamplona, Spain
Martinez-Pinilla, E:: Neuroscience Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain

Univ Navarra, Ctr Appl Med Res CIMA, Neurosci Dept, Pamplona, Spain
Sandoval, J:: Instituto de Investigación. Laboratory of Personalized Medicine, Epigenomics Unit, Medical Research Institute La Fe, Valencia, Spain

Instituto de Investigación. Med Res Inst La Fe, Epigen Unit, Lab Personalized Med, Valencia, Spain
Franco, R:: Laboratory of Molecular Neurobiology, Department of Biochemistry and Molecular Biomedicine, Faculty of Biology, University of Barcelona, Barcelona, Spain

Centro de Investigación en Red, Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain

Univ Barcelona, Dept Biochem & Mol Biomed, Mol Neurobiol Lab, Fac Biol, Barcelona, Spain

Inst Salud Carlos III, Ctr Invest Red Enfermedades Neurodegenera CIBERNE, Madrid, Spain
Perez-Mediavilla, A:: Neuroscience Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain

Department of Biochemistry and Genetics, School of Sciences, University of Navarra, Pamplona, Spain

Univ Navarra, Ctr Appl Med Res CIMA, Neurosci Dept, Pamplona, Spain

Univ Navarra, Sch Sci, Dept Biochem & Genet, Pamplona, Spain