Haplotype structure of the 17 q 21 region in progressive supranuclear palsy and corticobasal degeneration

Title 1 4 Brendza 20 23 Hartman Age-independent and age-dependent learning and memory abnormalities in PDAPP mice on a C57Bl/6 background 21 24 Hecimovic Mutagenesis of APP Reveals No Correlation Between Aβ and AICD Production 22 25 Holtzman In Vitro and In Vivo Characterization of Beta-Amyloid Antibodies Binding to Cerebral Amyloid Angiopathy (CAA) and the Selective Exacerbation of CAA-Associated Microhemorrhage 23 26 Holtzman Plasma Aβ Levels Following Aβ Antibody Administration in Young Mice Predicts Brain Amyloid Burden at an Older Age 24 27 Hosto The Influence of Depression in the Prediction of Cognitive Performance in Persons with DAT 25 28 Hu Identification of biomarkers for Alzheimer's disease using proteomics approaches 26 29 Kopan Is Substrate Oligomerization Regulating Cleavage by gamma-Secretase? 27 30 Mach Labeling Amyloid Plaque-like Structures by Radioiodinated Ligands in Rhesus Monkey Brain 28 31 Morris The Neuropathology of Nondemented Aging 29 32 Morris Is MCI Early Alzheimer's Disease? 30 33 Nowotny Linkage analysis of AD sib pairs indicates evidence of interaction between genes regulating beta-amyloid degradation 31 34 Nowotny Association of late onset Alzheimer's disease with genetic variation in multiple members of a gene family involved in neuronal apoptosis 32 35 Nowotny Genetic association studies of insulin-degrading enzyme (IDE) with late onset Alzheimer's disease (LOAD)-equivocal results from two large case-control studies 45 48 Zerbinatti Neuronal overexpression of LRP selectively increases a detergent-soluble pool of hippocampal Abeta in PDAPP mice 4 1 st WU Author Abstract (Presenting Author in Bold Type) Brendza P2-063 Background: Neuritic plaques are one of the defining features of Alzheimer's disease (AD) pathology. These structures are composed of extracellular accumulations of amyloid-β peptide (Aβ) and other plaque-associated proteins surrounded by large, swollen degenerating axons and dendrites (dystrophic neurites) and activated glial cells. Dystrophic neurites are thought to disrupt neuronal function, but whether damage to affected neurites is static, dynamic or reversible is unknown. Objective(s): We are studying the dynamics of neurite-amyloid interactions and characterizing the properties of amyloid toxicity in vivo, using a transgenic mouse model of AD. We are using our system to investigate whether dystrophic neurites undergo dynamic changes over time and if reducing both soluble and insoluble Aβ will promote the rapid recovery of amyloid-associated neuritic dystrophy. Methods: We are analyzing neuritic plaques in the brains of living PDAPP; Thy-1:YFP transgenic mice, a transgenic mouse model that develops AD-like pathology and also stably expresses yellow fluorescent protein (YFP) in a subset of …