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Yet, TE quantitative trait loci (teQTL) have not been well characterized in human aged brains with AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>We leveraged large\u2010scale bulk and single\u2010cell RNA sequencing, whole\u2010genome sequencing (WGS), and xQTL from three human AD brain biobanks to characterize TE expression dysregulation and experimentally validate AD\u2010associated TEs using CRISPR interference (CRISPRi) assays in human induced pluripotent stem cell (iPSC)\u2013derived neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      We identified 26,188 genome\u2010wide significant TE expression QTLs (teQTLs) in human aged brains. Subsequent colocalization analysis of teQTLs with AD genetic loci identified AD\u2010associated teQTLs and linked locus TEs. Using CRISPRi assays, we pinpointed a neuron\u2010specific suppressive role of the activated short interspersed nuclear element (SINE; chr11:47608036\u201347608220) on expression of\n                      <jats:italic>C1QTNF4<\/jats:italic>\n                      via reducing neuroinflammation in human iPSC\u2010derived neurons.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>We identified widespread TE dysregulation in human AD brains and teQTLs offer a complementary analytic approach to identify likely AD risk genes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Widespread transposable element (TE) dysregulations are observed in human aging brains with degrees of neuropathology, apolipoprotein E (\n                            <jats:italic>APOE<\/jats:italic>\n                            ) genotypes, and neuroinflammation in Alzheimer's disease (AD).\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>A catalog of TE quantitative trait loci (teQTLs) in human aging brains was created using matched RNA sequencing and whole\u2010genome sequencing data.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            CRISPR interference assays reveal that an upregulated intergenic TE from the\n                            <jats:italic>MIR<\/jats:italic>\n                            family (chr11: 47608036\u201347608220) suppresses expression of its nearest anti\u2010inflammatory gene\n                            <jats:italic>C1QTNF4<\/jats:italic>\n                            in human induced pluripotent stem cell\u2013derived neurons.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.14164","type":"journal-article","created":{"date-parts":[[2024,10,2]],"date-time":"2024-10-02T07:00:27Z","timestamp":1727852427000},"page":"7495-7517","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Widespread transposable element dysregulation in human aging brains with Alzheimer's disease"],"prefix":"10.1002","volume":"20","author":[{"given":"Yayan","family":"Feng","sequence":"first","affiliation":[{"name":"Cleveland Clinic Genome Center Lerner Research Institute Cleveland Clinic  Cleveland Ohio USA"},{"name":"Genomic Medicine 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