We are analyzing https://link.springer.com/article/10.1007/s40142-014-0034-x.

Title:
Late-Onset Alzheimer’s Disease Genes and the Potentially Implicated Pathways | Current Genetic Medicine Reports
Description:
Late-onset Alzheimer’s disease (LOAD) is a devastating neurodegenerative disease with no effective treatment or cure. In addition to APOE, recent large genome-wide association studies have identified variation in over 20 loci that contribute to disease risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA-DRB1/HLA-DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4. In addition, rare variants associated with LOAD have also been identified in APP, TREM2 and PLD3 genes. Previous research has identified inflammatory response, lipid metabolism and homeostasis, and endocytosis as the likely modes through which these gene products participate in Alzheimer’s disease. Despite the clustering of these genes across a few common pathways, many of their roles in disease pathogenesis have yet to be determined. In this review, we examine both general and postulated disease functions of these genes and consider a comprehensive view of their potential roles in LOAD risk.
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Keywords {🔍}

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Topics {✒️}

linking g-protein-coupled receptors raftk/pyk2-mediated cellular signalling hla-drb1/hla-drb5 locus potassium-dependent sodium/calcium exchanger atp-binding cassette transporter member 4a/membrane-spanning 4-domains genome-wide association studies genome-wide association study potassium depletion-induced apoptosis genome-wide association analysis hla-drb1/hla-drb5 sodium/potassium/calcium exchanger genome-wide significant locus pyk2/src-family kinase pathway abca7 [atp-binding cassette atp-binding cassette genes glial-derived neurotrophic factor atp-binding cassette subfamily article download pdf plasmacytoid dendritic cells nmda receptor current deep-learning–based prediction low-grade diffuse astrocytomas mediates tau-induced neurotoxicity destabilizes pro-apoptotic mrnas cell–matrix adhesion complexes central nervous system table 1 late-onset alzheimer α-synuclein-induced activation keywords late-onset alzheimer cell-mediated immune mechanisms ephrin/eph receptor signaling cell–cell adhesion complexes cas protein family genome-wide significant age-related cognitive decline clathrin adaptor calm/picalm increased steady-state levels sorl1 [sortilin-related receptor α-synuclein-induced neurodegeneration high-affinity ige receptor ephrin-eph receptor interactions ptpalpha-deficient mouse synaptosomes hodgkin reed-sternberg cells late-onset alzheimer disease implicates tau-mediated mechanisms cas family proteins potentially implicated pathways cas family member protein tyrosine receptors

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Late-Onset Alzheimer’s Disease Genes and the Potentially Implicated Pathways
         description:Late-onset Alzheimer’s disease (LOAD) is a devastating neurodegenerative disease with no effective treatment or cure. In addition to APOE, recent large genome-wide association studies have identified variation in over 20 loci that contribute to disease risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA-DRB1/HLA-DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4. In addition, rare variants associated with LOAD have also been identified in APP, TREM2 and PLD3 genes. Previous research has identified inflammatory response, lipid metabolism and homeostasis, and endocytosis as the likely modes through which these gene products participate in Alzheimer’s disease. Despite the clustering of these genes across a few common pathways, many of their roles in disease pathogenesis have yet to be determined. In this review, we examine both general and postulated disease functions of these genes and consider a comprehensive view of their potential roles in LOAD risk.
         datePublished:2014-03-22T00:00:00Z
         dateModified:2014-03-22T00:00:00Z
         pageStart:85
         pageEnd:101
         sameAs:https://doi.org/10.1007/s40142-014-0034-x
         keywords:
            Late-onset Alzheimer’s disease
            Genetics
            Biological pathways
            Internal Medicine
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                     name:University of Pittsburgh
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                        name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
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ScholarlyArticle:
      headline:Late-Onset Alzheimer’s Disease Genes and the Potentially Implicated Pathways
      description:Late-onset Alzheimer’s disease (LOAD) is a devastating neurodegenerative disease with no effective treatment or cure. In addition to APOE, recent large genome-wide association studies have identified variation in over 20 loci that contribute to disease risk: CR1, BIN1, INPP5D, MEF2C, TREM2, CD2AP, HLA-DRB1/HLA-DRB5, EPHA1, NME8, ZCWPW1, CLU, PTK2B, PICALM, SORL1, CELF1, MS4A4/MS4A6E, SLC24A4/RIN3,FERMT2, CD33, ABCA7, CASS4. In addition, rare variants associated with LOAD have also been identified in APP, TREM2 and PLD3 genes. Previous research has identified inflammatory response, lipid metabolism and homeostasis, and endocytosis as the likely modes through which these gene products participate in Alzheimer’s disease. Despite the clustering of these genes across a few common pathways, many of their roles in disease pathogenesis have yet to be determined. In this review, we examine both general and postulated disease functions of these genes and consider a comprehensive view of their potential roles in LOAD risk.
      datePublished:2014-03-22T00:00:00Z
      dateModified:2014-03-22T00:00:00Z
      pageStart:85
      pageEnd:101
      sameAs:https://doi.org/10.1007/s40142-014-0034-x
      keywords:
         Late-onset Alzheimer’s disease
         Genetics
         Biological pathways
         Internal Medicine
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                     type:PostalAddress
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            type:Person
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                  name:University of Pittsburgh
                  address:
                     name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
                     type:PostalAddress
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                  name:University of Pittsburgh
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                     name:Alzheimer’s Disease Research Center, University of Pittsburgh, Pittsburgh, USA
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Person:
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      affiliation:
            name:University of Pittsburgh
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               name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
               type:PostalAddress
            type:Organization
      name:M. Ilyas Kamboh
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               name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
               type:PostalAddress
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            address:
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      name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
      name:Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA
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