Abstract

The accumulation of the toxic Aβ peptide in Alzheimer's disease (AD) largely relies upon an efficient recycling of amyloid precursor protein (APP). Recent genetic association studies have described rare variants in SORL1 with putative pathogenic consequences in the recycling of APP. In this work, we examine the presence of rare coding variants in SORL1 in three different European American cohorts: early-onset, late-onset AD (LOAD) and familial LOAD.

Original languageEnglish
Pages (from-to)1828-1830
Number of pages3
JournalEuropean Journal of Human Genetics
Volume24
Issue number12
DOIs
StatePublished - Dec 1 2016

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