Apolipoprotein A-I Deficiency Increases Cerebral Amyloid Angiopathy and Cognitive Deficits in APP/PS1ΔE9 Mice
Open Access
- 1 November 2010
- journal article
- Published by Elsevier BV
- Vol. 285 (47), 36945-36957
- https://doi.org/10.1074/jbc.m110.127738
Abstract
No abstract availableThis publication has 56 references indexed in Scilit:
- Overexpression of Human Apolipoprotein A-I Preserves Cognitive Function and Attenuates Neuroinflammation and Cerebral Amyloid Angiopathy in a Mouse Model of Alzheimer DiseasePublished by Elsevier BV ,2010
- EGCG remodels mature α-synuclein and amyloid-β fibrils and reduces cellular toxicityProceedings of the National Academy of Sciences of the United States of America, 2010
- Fibrillar Oligomers Nucleate the Oligomerization of Monomeric Amyloid β but Do Not Seed Fibril FormationJournal of Biological Chemistry, 2010
- Role of HDL, ABCA1, and ABCG1 Transporters in Cholesterol Efflux and Immune ResponsesArteriosclerosis, Thrombosis, and Vascular Biology, 2010
- Memory Deficits in APP23/Abca1+/−Mice Correlate with the Level of AβOligomersASN Neuro, 2009
- Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s diseaseActa Neuropathologica, 2009
- Selective targeting of perivascular macrophages for clearance of β-amyloid in cerebral amyloid angiopathyProceedings of the National Academy of Sciences of the United States of America, 2009
- Structural Classification of Toxic Amyloid OligomersJournal of Biological Chemistry, 2008
- Soluble oligomers of the amyloid β-protein impair synaptic plasticity and behaviorBehavioural Brain Research, 2008
- Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of PathogenesisScience, 2003