title: Dissecting risk haplotypes in sporadic Alzheimer's disease.
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.
authors.affiliation: The Whitehead Institute, 9 Cambridge Center, Cambridge, MA 02142, USA. Electronic address: soldner@wi.mit.edu.
authors.forename: Frank
authors.initials: F
authors.lastname: Soldner
authors.affiliation: 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.
authors.forename: Rudolf
authors.initials: R
authors.lastname: Jaenisch
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics*; D006801:Humans; D057026:Induced Pluripotent Stem Cells / Q000502:physiology*; D026502:LDL-Receptor Related Proteins / Q000235:genetics*; D026901:Membrane Transport Proteins / Q000235:genetics*; D009474:Neurons / Q000502:physiology*; D000685:Serum Amyloid A Protein / Q000378:metabolism*
chemical_list: D026502:LDL-Receptor Related Proteins; D026901:Membrane Transport Proteins; D000685:Serum Amyloid A Protein