scispace - formally typeset
P

Peter St George-Hyslop

Researcher at University of Cambridge

Publications -  385
Citations -  44145

Peter St George-Hyslop is an academic researcher from University of Cambridge. The author has contributed to research in topics: Presenilin & Amyloid precursor protein. The author has an hindex of 90, co-authored 366 publications receiving 39483 citations. Previous affiliations of Peter St George-Hyslop include Washington University in St. Louis & Russian Academy.

Papers
More filters
Journal ArticleDOI

Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease

Jean-Charles Lambert, +215 more
- 01 Dec 2013 - 
TL;DR: In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
Journal ArticleDOI

Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease.

Adam C. Naj, +156 more
- 01 May 2011 - 
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
Journal ArticleDOI

Gene-wide analysis detects two new susceptibility genes for Alzheimer's disease.

Valentina Escott-Price, +194 more
- 12 Jun 2014 - 
TL;DR: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimers disease.
Journal ArticleDOI

Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease

TL;DR: Aβ immunization reduces both deposition of cerebral fibrillar Aβ and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of Aβ in the brain, which implies that either a ∼50% reduction in dense-cored Aβ plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic Aβ species.