ArticleAnnals of neurology2011
SORCS1 alters amyloid precursor protein processing and variants may increase Alzheimer's disease risk.
Article in Annals of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 3 of them syntheses that pooled it.
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Who cites it
77 citing papers in PubMed, 3 syntheses or guidelines pooled it, 120 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- MiR-574-5P, miR-1827, and miR-4429 as Potential Biomarkers for Schizophrenia.Journal of molecular neuroscience : MN · 2022Pooled it
- Impact of genetic variation in SORCS1 on memory retention.PloS one · 2011Pooled it
- Golgi dysfunction in Alzheimer disease: from human multiomic signatures to therapeutic targets.Experimental & molecular medicine · 2026Review
- Transcriptional signature of induced neurons differentiates virologically suppressed people with HIV from people without HIV.JCI insight · 2026Article
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- Large-scale meta- and cross-trait analyses uncover shared genetic risk factors for IBS and psychiatric disorders.Frontiers in psychiatry · 2026Article
- Identification of SORCS1 as a candidate gene associated with canine behavioral traits: Insights from guide dog training outcomes.PloS one · 2026Article
- NFκB1: a common biomarker linking Alzheimer's and Parkinson's disease pathology.Frontiers in neuroscience · 2025Article
- Whole-genome sequencing study in Koreans identifies novel loci for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- A Transcriptional Signature of Induced Neurons Differentiates Virologically Suppressed People Living With HIV from People Without HIV.bioRxiv : the preprint server for biology · 2024Article
- Unraveling the genetic architecture of blood unfolded p-53 among non-demented elderlies: novel candidate genes for early Alzheimer's disease.BMC genomics · 2024Article
- Proteomic Analysis to Identify Prospective Biomarkers of Treatment Outcome After Microvascular Decompression for Trigeminal Neuralgia: A Preliminary Study.The journal of pain · 2024Article
- Genetics of Alzheimer's Disease in the African American Population.Journal of clinical medicine · 2023Review
- Converging links between adult-onset neurodegenerative Alzheimer's disease and early life neurodegenerative neuronal ceroid lipofuscinosis?Neural regeneration research · 2023Review
- SorCS1 inhibits amyloid-β binding to neurexin and rescues amyloid-β-induced synaptic pathology.Life science alliance · 2023Article
- Multimodal data integration via mediation analysis with high-dimensional exposures and mediators.Human brain mapping · 2022Article
- CpH methylome analysis in human cortical neurons identifies novel gene pathways and drug targets for opioid use disorder.Frontiers in psychiatry · 2022Article
- Beware of Misdelivery: Multifaceted Role of Retromer Transport in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2022Review
- SorCS2 is required for social memory and trafficking of the NMDA receptor.Molecular psychiatry · 2021Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 9 institutions in 6 countries.
Funding
Abstract
objectiveSorting mechanisms that cause the amyloid precursor protein (APP) and the β-secretases and γ-secretases to colocalize in the same compartment play an important role in the regulation of Aβ production in Alzheimer's disease (AD). We and others have reported that genetic variants in the Sortilin-related receptor (SORL1) increased the risk of AD, that SORL1 is involved in trafficking of APP, and that underexpression of SORL1 leads to overproduction of Aβ. Here we explored the role of one of its homologs, the sortilin-related VPS10 domain containing receptor 1 (SORCS1), in AD.
methodsWe analyzed the genetic associations between AD and 16 SORCS1-single nucleotide polymorphisms (SNPs) in 6 independent data sets (2,809 cases and 3,482 controls). In addition, we compared SorCS1 expression levels of affected and unaffected brain regions in AD and control brains in microarray gene expression and real-time polymerase chain reaction (RT-PCR) sets, explored the effects of significant SORCS1-SNPs on SorCS1 brain expression levels, and explored the effect of suppression and overexpression of the common SorCS1 isoforms on APP processing and Aβ generation.
resultsInherited variants in SORCS1 were associated with AD in all datasets (0.001 < p < 0.049). In addition, SorCS1 influenced APP processing. While overexpression of SorCS1 reduced γ-secretase activity and Aβ levels, the suppression of SorCS1 increased γ-secretase processing of APP and the levels of Aβ. INTERPRETATIONS: These data suggest that inherited or acquired changes in SORCS1 expression or function may play a role in the pathogenesis of AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.