Dissecting risk haplotypes in sporadic Alzheimer's disease

Frank Soldner; Rudolf Jaenisch

doi:10.1016/j.stem.2015.03.010

Dissecting risk haplotypes in sporadic Alzheimer's disease

Cell Stem Cell. 2015 Apr 2;16(4):341-2. doi: 10.1016/j.stem.2015.03.010.

Authors

Frank Soldner¹, Rudolf Jaenisch²

Affiliations

¹ The Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02142, USA. Electronic address: soldner@wi.mit.edu.
² The Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, 31 Ames Street, Cambridge, MA 02139, USA. Electronic address: jaenisch@wi.mit.edu.

PMID: 25842969
DOI: 10.1016/j.stem.2015.03.010

Abstract

Understanding how genetic risk variants contribute to complex diseases is crucial for predicting disease susceptibility and developing patient-tailored therapies. In this issue of Cell Stem Cell, Young et al. (2015) dissect the function of common non-coding risk haplotypes in the SORL1 locus in the pathogenesis of sporadic Alzheimer's disease using patient-derived induced pluripotent stem cells.

Publication types

Comment

MeSH terms

Alzheimer Disease / genetics*
Humans
Induced Pluripotent Stem Cells / physiology*
LDL-Receptor Related Proteins / genetics*
Membrane Transport Proteins / genetics*
Neurons / physiology*
Serum Amyloid A Protein / metabolism*

Substances

LDL-Receptor Related Proteins
Membrane Transport Proteins
Serum Amyloid A Protein

Grants and funding

R01 CA084198/CA/NCI NIH HHS/United States