{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T03:40:21Z","timestamp":1792554021337,"version":"4.5.0"},"reference-count":141,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T00:00:00Z","timestamp":1792454400000},"content-version":"vor","delay-in-days":19,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"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":[[2026,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>Epigenetic dysregulation is increasingly linked to aging and neurodegeneration, yet its contribution to retinal and brain pathology in Alzheimer's disease (AD) remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      We quantified the repressive epigenetic mark histone H3 lysine 9 trimethylation (H3K9me3) in\n                      <jats:italic>post mortem<\/jats:italic>\n                      retinas and brains from donors spanning normal cognition, mild cognitive impairment, and AD dementia. Using a multi\u2010enzyme methyltransferase panel, we characterized the in vitro inhibitory activity of ETP69, an epidithiodiketopiperazine, against suppressor of variegation 3\u20109 homologue 1 (SUV39H1) and other methyltransferases. In two transgenic AD mouse models (APPswe\/PS1dE9 and APPswe\/tauP301L\/PS1\n                      <jats:italic>\n                        <jats:sup>tm1Mpm<\/jats:sup>\n                      <\/jats:italic>\n                      ), we assessed ETP69 effects on cerebral H3 methylation, behavior, AD\u2010like pathology, synaptic integrity, and proteomic profiles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      H3K9me3 increased early across the AD continuum in both brain and retina, correlating with cognitive impairment and neuropathological burden. H3K9me3 levels were strongly correlated between matched brains and retinas (\n                      <jats:italic>r<\/jats:italic>\n                      \u00a0=\u00a00.72,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a00.0002). ETP69 substantially inhibited SUV39H1 and several other methyltransferases in cell\u2010free assays, while consistently reducing cerebral H3K9me3 in vivo relative to other histone marks assessed. In mice, pharmacological H3K9me3 reduction mitigated AD\u2010like pathology, preserved synapses, and improved short\u2010 and long\u2010term cognitive and visual performance. Proteomics revealed that H3K9me3 derepression re\u2010established retinal and brain proteostasis and remodeled innate immune pathways and brain\u2010derived neurotrophic factor\/nerve growth factor\u2010inducible protein (BDNF\/VGF)\u2013granin signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>This study identifies H3K9me3 accumulation as a shared, reversible epigenetic contributor to AD across the retina\u2013brain axis; its reduction represents a promising disease\u2010modifying strategy, and the retina may provide an accessible readout of brain epigenetic dysfunction.<\/jats:p>\n                  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