Physiologically regulated transgenic ABCA1 does not reduce amyloid burden or amyloid-β peptide levels in vivo
Open Access
- 1 April 2007
- journal article
- Published by Elsevier BV in Journal of Lipid Research
- Vol. 48 (4), 914-923
- https://doi.org/10.1194/jlr.m600543-jlr200
Abstract
No abstract availableKeywords
This publication has 52 references indexed in Scilit:
- The effects of ABCA1 on cholesterol efflux and Aβ levels in vitro and in vivoJournal of Neurochemistry, 2006
- ABCA1 Is Required for Normal Central Nervous System ApoE Levels and for Lipidation of Astrocyte-secreted apoEPublished by Elsevier BV ,2004
- Deficiency of ABCA1 Impairs Apolipoprotein E Metabolism in BrainPublished by Elsevier BV ,2004
- Co-localization of cholesterol, apolipoprotein E and fibrillar Aβ in amyloid plaquesMolecular Brain Research, 2003
- Senile plaque composition and posttranslational modification of amyloid-β peptide and associated proteinsPeptides, 2002
- Human and Murine ApoE Markedly Alters Aβ Metabolism before and after Plaque Formation in a Mouse Model of Alzheimer's DiseaseNeurobiology of Disease, 2002
- New Frontiers in Alzheimer's Disease GeneticsNeuron, 2001
- Lipoproteins in the Central Nervous SystemAnnals of the New York Academy of Sciences, 2000
- Apolipoprotein E is essential for amyloid deposition in the APP V717F transgenic mouse model of Alzheimer's diseaseProceedings of the National Academy of Sciences of the United States of America, 1999
- Lack of apolipoprotein E dramatically reduces amyloid β-peptide depositionNature Genetics, 1997