Comparison of Aβ levels in the brain of familial and sporadic Alzheimer's disease
- 1 September 2009
- journal article
- research article
- Published by Elsevier in Neurochemistry International
- Vol. 55 (4) , 243-252
Abstract
No abstract availableKeywords
This publication has 73 references indexed in Scilit:
- Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memoryNature Medicine, 2008
- Loss‐of‐function presenilin mutations in Alzheimer diseaseEMBO Reports, 2007
- The presenilin hypothesis of Alzheimer's disease: Evidence for a loss-of-function pathogenic mechanismProceedings of the National Academy of Sciences, 2007
- Mean age of onset in familial Alzheimer's disease is determined by amyloid beta 42Neurobiology of Aging, 2005
- Enhanced generation of intracellular Aβ42 amyloid peptide by mutation of presenilins PS1 and PS2European Journal of Neuroscience, 2004
- Prospective Belgian study of neurodegenerative and vascular dementia: APOE genotype effectsJournal of Neurology, Neurosurgery & Psychiatry, 2003
- α‐Secretase‐Derived Product of β‐Amyloid Precursor Protein Is Decreased by Presenilin 1 Mutations Linked to Familial Alzheimer's DiseaseJournal of Neurochemistry, 1997
- Amyloid β protein (Aβ) deposition in chromosome 14–linked Alzheimer's disease: Predominance of Aβ42(43)Annals of Neurology, 1996
- Chromosome 14–encoded Alzheimer's disease: Genetic and clinicopathological descriptionAnnals of Neurology, 1994
- Clinical diagnosis of Alzheimer's diseaseNeurology, 1984