Complement activation and β-amyloid-mediated neurotoxicity in Alzheimer's disease
- 31 December 1992
- journal article
- review article
- Published by Elsevier in Research in Immunology
- Vol. 143 (6), 624-630
- https://doi.org/10.1016/0923-2494(92)80046-n
Abstract
No abstract availableThis publication has 20 references indexed in Scilit:
- Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein geneNature, 1991
- Immunohistochemical localization of vitronectin, its receptor and beta-3 integrin in Alzheimer brain tissueJournal of Neuroimmunology, 1991
- Detection of the membrane inhibitor of reactive lysis (CD59) in diseased neurons of Alzheimer brainBrain Research, 1991
- Dynamics of gene expression for a hippocampal glycoprotein elevated in Alzheimer's disease and in response to experimental lesions in ratNeuron, 1990
- β-Amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damageBrain Research, 1990
- Presence of T-cytotoxic suppressor and leucocyte common antigen positive cells in Alzheimer's disease brain tissueNeuroscience Letters, 1988
- The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptorNature, 1987
- Autoantibodies to neurofibrillary tangles and brain tissue in Alzheimer's disease. Establishment of Epstein-Barr virus-transformed antibody-producing cell lines.The Journal of Experimental Medicine, 1987
- The Classical Complement Pathway: Activation and Regulation of the First Complement ComponentAdvances in Immunology, 1985
- Alzheimer's disease and Down's syndrome: Sharing of a unique cerebrovascular amyloid fibril proteinBiochemical and Biophysical Research Communications, 1984