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Perinatal Choline Supplementation Reduces Amyloidosis and Increases Cholinergic Marker Expression in the Hippocampus of the APPswePS1dE9 Alzheimer's Disease Model Mice
Author(s) -
Mellott Tiffany,
Huleatt Olivia,
Shade Bethany,
Pender Sarah,
Liu Yi Bessie,
Blusztajn Jan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.900.1
Subject(s) - choline acetyltransferase , endocrinology , choline , hippocampus , offspring , medicine , weaning , alzheimer's disease , astrogliosis , amyloid precursor protein , cholinergic , biology , amyloidosis , disease , pregnancy , central nervous system , genetics
Prevention of Alzheimer's disease (AD) is a major goal of biomedical sciences. In previous studies we showed that high intake of the essential nutrient, choline, during gestation prevented age‐related memory decline in a rat model. In this study we investigated the effects of a similar treatment on AD‐related phenotypes in a mouse model of AD. We crossed wild type female mice with hemizygous APPswe.PS1dE9 (APP.PS1) AD model male mice and maintained the pregnant and lactating dams on a control AIN76A diet containing 8 mmol/kg of choline or a choline supplemented (36 mmol/kg) diet. After weaning all offspring consumed the control diet. As compared to APP.PS1 mice reared on the control diet, the hippocampus of the perinatally choline supplemented APP.PS1 mice exhibited: 1) reduced levels of solubilized amyloid Aβ40 and Aβ42 peptides; 2) reduced number and total area of amyloid plaques; 3) preserved levels of choline acetyltransferase protein and 4) absence of astrogliosis. The data suggest that dietary supplementation of choline during fetal development and early postnatal life may constitute a preventive strategy for AD. Supported by BUADC pilot grant and NIRG‐10‐17273 from the Alzheimer's Association to TJM