The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease

By E. Rogaeva, Y. Meng, Joseph H. Lee, Yongjun Gu, T. Kawarai, F. Zou, Taiichi Katayama, C. Baldwin, R. Cheng, H. Hasegawa and 31 more. Nature Genetics, 2007

1,212 citations recorded by the source corpus.

Subfields: Cell Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/e27a71626bceae762ec497714651d6d92160ec15

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. G. Bu
2. D. Holtzman
3. D. Selkoe
4. Burkhard Rost

In Neurology

1. P. Reddy
2. D. Selkoe
3. Christian Haass
4. John Hardy
5. M. Beal
6. Rudolph E. Tanzi
7. G. Bu
8. Sangram S. Sisodia

In Physiology

1. D. Holtzman
2. G. Bu
3. J. Herz
4. P. Reddy
5. D. Selkoe
6. M. Beal
7. John Hardy
8. Rudolph E. Tanzi

Citations in the corpus

• Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy (2009, background): “More direct evidence linking SORLA to AD comes from a recent study which demonstrated that inherited variants in the SORL1 gene are associated with LOA”
• The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “In accord, one of the numerous risk genes for late-onset AD is PICALM, and AD-promoting alleles or knockdown of this gene has been shown to decrease Ab clearance across the brain endothelium (Zhao et al 2015).”
• Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “Apolipoprotein E gene allele 4 (ApoE4) genotype [17] and a genetic variant in the sortilinrelated receptor 1 gene [18] are risk factors for developing late-onset AD.”
• Trafficking and proteolytic processing of APP. (2012, background): “…et al. 2006). sorLA/LR11 is also genetically associatedwith AD and its steady-state levels are markedly reduced in the brains of patients with AD, further implicating this sortingmolecule in the physiological regulation of APPmetabolism (Andersen et al. 2005; Offe et al. 2006; Rogaeva et al. 2007).”
• Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “Overexpression of SORLA in neuronal cells can block amyloidogenic processing and reduce Aβ production [485], whereas loss of SORLA increased extracellular Aβ levels and plaque deposition in several AD mouse models [486, 487].”
• The genetics of Alzheimer disease: back to the future. (2010, background): “…reductase; Chapman et al., 1998), OTC (ornithine carbamoyltransferase; Bensemain et al., 2009), SORL1 (sortilin-related receptor; Rogaeva et al., 2007), and TF (transferrin; van Rensburg et al., 1993), which all show modest genetic effects but only modest statistical support in…”
• Epidemiology of Alzheimer Disease (2012, neutral): “Although in line with other recently described genetic links for AD (Lee et al. 2007; Rogaeva et al. 2007), the effect sizes of the SORL1 associations are modest (Reitz et al.”
• Alzheimer's disease risk genes and mechanisms of disease pathogenesis (2014, neutral): “SORL1 was originally identified as an AD risk gene in candidate-based approaches (134,135).”