Article: The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease
| Title | The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease |
|---|---|
| Authors | Rogaeva, E7 13 Meng, Y5 9 Lee, JH10 15 Gu, Y7 13 Kawarai, T7 13 Zou, F1 4 Katayama, T7 13 Baldwin, CT5 9 Cheng, R10 15 Hasegawa, H7 13 Chen, F7 13 Shibata, N7 13 Lunetta, KL5 9 PardossiPiquard, R7 13 Bohm, C7 13 Wakutani, Y7 13 Cupples, LA5 9 Cuenco, KT5 9 Green, RC5 9 Pinessi, L6 Rainero, I6 Sorbi, S8 Bruni, A17 Duara, R3 16 Friedland, RP11 Inzelberg, R18 Hampe, W14 Bujo, H19 Song, YQ2 Andersen, OM12 Willnow, TE12 GraffRadford, N4 Petersen, RC4 Dickson, D4 Der, SD7 13 Fraser, PE7 13 SchmittUlms, G7 13 Younkin, S4 Mayeux, R10 15 Farrer, LA5 15 St GeorgeHyslop, P7 13 |
| Issue Date | 2007 |
| Publisher | Nature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com |
| Citation | Nature Genetics, 2007, v. 39 n. 2, p. 168-177 [How to Cite?] DOI: http://dx.doi.org/10.1038/ng1943 |
| Abstract | The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid Β peptide (AΒ) in Alzheimer disease. We report here that inherited variants in the SORL1 neuronal sorting receptor are associated with late-onset Alzheimer disease. These variants, which occur in at least two different clusters of intronic sequences within the SORL1 gene (also known as LR11 or SORLA) may regulate tissue-specific expression of SORL1. We also show that SORL1 directs trafficking of APP into recycling pathways and that when SORL1 is underexpressed, APP is sorted into AΒ-generating compartments. These data suggest that inherited or acquired changes in SORL1 expression or function are mechanistically involved in causing Alzheimer disease. © 2007 Nature Publishing Group. |
| ISSN | 1061-4036 2011 Impact Factor: 35.532 2011 SCImago Journal Rankings: 8.923 |
| DOI | http://dx.doi.org/10.1038/ng1943 |
| ISI Accession Number ID | WOS:000244063900014 |
| References | References in Scopus |
| dc.contributor.author | Rogaeva, E |
|---|---|
| dc.contributor.author | Meng, Y |
| dc.contributor.author | Lee, JH |
| dc.contributor.author | Gu, Y |
| dc.contributor.author | Kawarai, T |
| dc.contributor.author | Zou, F |
| dc.contributor.author | Katayama, T |
| dc.contributor.author | Baldwin, CT |
| dc.contributor.author | Cheng, R |
| dc.contributor.author | Hasegawa, H |
| dc.contributor.author | Chen, F |
| dc.contributor.author | Shibata, N |
| dc.contributor.author | Lunetta, KL |
| dc.contributor.author | PardossiPiquard, R |
| dc.contributor.author | Bohm, C |
| dc.contributor.author | Wakutani, Y |
| dc.contributor.author | Cupples, LA |
| dc.contributor.author | Cuenco, KT |
| dc.contributor.author | Green, RC |
| dc.contributor.author | Pinessi, L |
| dc.contributor.author | Rainero, I |
| dc.contributor.author | Sorbi, S |
| dc.contributor.author | Bruni, A |
| dc.contributor.author | Duara, R |
| dc.contributor.author | Friedland, RP |
| dc.contributor.author | Inzelberg, R |
| dc.contributor.author | Hampe, W |
| dc.contributor.author | Bujo, H |
| dc.contributor.author | Song, YQ |
| dc.contributor.author | Andersen, OM |
| dc.contributor.author | Willnow, TE |
| dc.contributor.author | GraffRadford, N |
| dc.contributor.author | Petersen, RC |
| dc.contributor.author | Dickson, D |
| dc.contributor.author | Der, SD |
| dc.contributor.author | Fraser, PE |
| dc.contributor.author | SchmittUlms, G |
| dc.contributor.author | Younkin, S |
| dc.contributor.author | Mayeux, R |
| dc.contributor.author | Farrer, LA |
| dc.contributor.author | St GeorgeHyslop, P |
| dc.date.accessioned | 2012-05-29T06:04:35Z |
| dc.date.available | 2012-05-29T06:04:35Z |
| dc.date.issued | 2007 |
| dc.description.abstract | The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid Β peptide (AΒ) in Alzheimer disease. We report here that inherited variants in the SORL1 neuronal sorting receptor are associated with late-onset Alzheimer disease. These variants, which occur in at least two different clusters of intronic sequences within the SORL1 gene (also known as LR11 or SORLA) may regulate tissue-specific expression of SORL1. We also show that SORL1 directs trafficking of APP into recycling pathways and that when SORL1 is underexpressed, APP is sorted into AΒ-generating compartments. These data suggest that inherited or acquired changes in SORL1 expression or function are mechanistically involved in causing Alzheimer disease. © 2007 Nature Publishing Group. |
| dc.description.nature | Link_to_subscribed_fulltext |
| dc.identifier.citation | Nature Genetics, 2007, v. 39 n. 2, p. 168-177 [How to Cite?] DOI: http://dx.doi.org/10.1038/ng1943 |
| dc.identifier.citeulike | 1044523 |
| dc.identifier.doi | http://dx.doi.org/10.1038/ng1943 |
| dc.identifier.epage | 177 |
| dc.identifier.isi | WOS:000244063900014 |
| dc.identifier.issn | 1061-4036 2011 Impact Factor: 35.532 2011 SCImago Journal Rankings: 8.923 |
| dc.identifier.issue | 2 |
| dc.identifier.pmid | 17220890 |
| dc.identifier.scopus | eid_2-s2.0-33846613222 |
| dc.identifier.spage | 168 |
| dc.identifier.uri | http://hdl.handle.net/10722/147558 |
| dc.identifier.volume | 39 |
| dc.language | eng |
| dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com |
| dc.publisher.place | United States |
| dc.relation.ispartof | Nature Genetics |
| dc.relation.references | References in Scopus |
| dc.subject.mesh | Age Of Onset |
| dc.subject.mesh | Alzheimer Disease - Genetics |
| dc.subject.mesh | Amyloid Beta-Peptides - Metabolism |
| dc.subject.mesh | Amyloid Beta-Protein Precursor - Metabolism |
| dc.subject.mesh | Cell Line |
| dc.subject.mesh | Endosomes - Metabolism |
| dc.subject.mesh | Genetic Variation |
| dc.subject.mesh | Haplotypes |
| dc.subject.mesh | Humans |
| dc.subject.mesh | Introns |
| dc.subject.mesh | Ldl-Receptor Related Proteins - Genetics |
| dc.subject.mesh | Membrane Transport Proteins - Genetics |
| dc.subject.mesh | Models, Genetic |
| dc.subject.mesh | Organ Specificity |
| dc.subject.mesh | Polymorphism, Single Nucleotide |
| dc.subject.mesh | Protease Nexins |
| dc.subject.mesh | Receptors, Cell Surface - Metabolism |
| dc.subject.mesh | Vesicular Transport Proteins - Metabolism |
| dc.title | The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease |
| dc.type | Article |
Author Affiliations
- Mayo Clinic in Rochester, Minnesota
- The University of Hong Kong
- Mount Sinai Medical Center Miami Beach
- Mayo Clinic in Jacksonville, Florida
- Boston University School of Public Health
- Università degli Studi di Torino
- Toronto Western Hospital
- Università degli Studi di Firenze
- Boston University School of Medicine
- Columbia University Medical Center
- Case Western Reserve University
- Max Delbruck Center for Molecular Medicine
- University of Toronto
- Universitätsklinikum Hamburg-Eppendorf und Medizinische Fakultät
- Columbia University, College of Physicians and Surgeons
- University of Miami Leonard M. Miller School of Medicine
- Regional Center of Neurogenetics
- The Ruth and Bruce Rappaport Faculty of Medicine
- Chiba University

