{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:38:35Z","timestamp":1792132715364,"version":"4.4.0"},"reference-count":161,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T00:00:00Z","timestamp":1752019200000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T00:00:00Z","timestamp":1751328000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp; Dementia"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>While RNA editing has been linked to Alzheimer's disease (AD), its specific impact on the transcriptomic landscape in human AD brains remains under explored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      We conducted a comprehensive analysis of RNA editing across nine human brain regions affected by AD, utilizing RNA\u2010seq data and matched whole\u2010genome sequencing data from three human brain biobanks, adjusting for age,\n                      <jats:italic>post mortem<\/jats:italic>\n                      interval, sex, and apolipoprotein E4 (\n                      <jats:italic>APOE4)<\/jats:italic>\n                      status.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      RNA\u2010editing events were identified in both AD and healthy control aging brains, highlighting 127 genes with significant RNA editing loci. AD exhibited elevated RNA editing in the parahippocampal gyrus and cerebellar cortex. We also discovered 147 colocalized genome\u2010wide association studies (GWAS) and\n                      <jats:italic>cis<\/jats:italic>\n                      \u2010edQTL (\u00b1\u00a01\u00a0MB) signals in 48 likely causal genes encompassing\n                      <jats:italic>CLU<\/jats:italic>\n                      ,\n                      <jats:italic>BIN1<\/jats:italic>\n                      , and\n                      <jats:italic>GRIN3B<\/jats:italic>\n                      , primarily allied to amyloid and tau pathology, and neuroinflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>Our findings delineate RNA editing regulatory signatures in human AD, providing novel insights into AD pathophysiology and potential biomarkers and therapeutic targets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"explicit-label\">\n                        <jats:list-item>\n                          <jats:p>\n                            We discovered genome\u2010wide landscape of RNA editing signals from 4208 (1364 Alzheimer's disease [AD] cases vs. 742 healthy controls) RNA\u2010seq data across nine human brain regions from three large brain biobanks (Mount Sinai Brain Bank [MSBB], Mayo Clinic [MAYO] Religious Order Study and Memory and Aging Project [ROSMAP]) tied with AD, including in sex\u2010specific and apolipoprotein E4 (APOE4) \u2010specific manner adjusting for age,\n                            <jats:italic>post mortem<\/jats:italic>\n                            interval (PMI), sex, and APOE4 status.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            We emphasize 127 genes, including\n                            <jats:italic>SYT11<\/jats:italic>\n                            ,\n                            <jats:italic>KCNIP4<\/jats:italic>\n                            ,\n                            <jats:italic>NRG3<\/jats:italic>\n                            ,\n                            <jats:italic>ANKS1B<\/jats:italic>\n                            , and\n                            <jats:italic>RALYL<\/jats:italic>\n                            , exhibiting significant RNA editing loci shared by multiple brain tissues, mainly implicated in synaptic plasticity, signaling and transmission, neuronal development, and morphogenesis.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Brain\u2010wide tissue\u2010specific\n                            <jats:italic>cis<\/jats:italic>\n                            \u2010regulatory variants (\n                            <jats:italic>cis<\/jats:italic>\n                            \u2010edQTLs) were inspected using matched genotyping data from 3627 samples from all brain biobanks. We revealed 147 colocalized AD\u2010GWAS and\n                            <jats:italic>cis<\/jats:italic>\n                            \u2010edQTLs signals pertaining to 48 likely causal genes comprising\n                            <jats:italic>CLU<\/jats:italic>\n                            (rs7982, rs1532278),\n                            <jats:italic>BIN1<\/jats:italic>\n                            (rs2276582, rs3768863),\n                            <jats:italic>GRIN3B<\/jats:italic>\n                            (rs10417824, rs1058603),\n                            <jats:italic>NYAP1<\/jats:italic>\n                            (rs12539172),\n                            <jats:italic>DGKQ<\/jats:italic>\n                            (rs4690197, rs3733347),\n                            <jats:italic>CLPTM1<\/jats:italic>\n                            (rs204468), etc.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Colocalized signals show affiliations to tau protein binding, amyloid\u2010\u03b2 regulation, cellular morphogenesis, and immune response pathway suggesting possible roles of epitranscriptomic mechanisms in shaping the AD risk.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.70452","type":"journal-article","created":{"date-parts":[[2025,7,9]],"date-time":"2025-07-09T13:52:09Z","timestamp":1752069129000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Comprehensive characterization of the RNA editing landscape in the human aging brains with Alzheimer's disease"],"prefix":"10.1002","volume":"21","author":[{"given":"Amit Kumar","family":"Gupta","sequence":"first","affiliation":[{"name":"Cleveland Clinic Genome Center Lerner Research 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