{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:08:47Z","timestamp":1790712527077,"version":"4.1.0"},"reference-count":83,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T00:00:00Z","timestamp":1701820800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2024,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>INTRODUCTION<\/jats:title>\n                    <jats:p>Early\u2010life stress (ES) increases the risk for Alzheimer's disease (AD). We and others have shown that ES aggravates amyloid\u2010beta (A\u03b2) pathology and promotes cognitive dysfunction in APP\/PS1 mice, but underlying mechanisms remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>We studied how ES affects the hippocampal synaptic proteome in wild\u2010type (WT) and APP\/PS1 mice at early and late pathological stages, and validated hits using electron microscopy and immunofluorescence.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>The hippocampal synaptosomes of both ES\u2010exposed WT and early\u2010stage APP\/PS1 mice showed a relative decrease in actin dynamics\u2010related proteins and a relative increase in mitochondrial proteins. ES had minimal effects on older WT mice, while strongly affecting the synaptic proteome of advanced stage APP\/PS1 mice, particularly the expression of astrocytic and mitochondrial proteins.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>Our data show that ES and amyloidosis share pathogenic pathways involving synaptic mitochondrial dysfunction and lipid metabolism, which may underlie the observed impact of ES on the trajectory of AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.13569","type":"journal-article","created":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T21:24:08Z","timestamp":1701897848000},"page":"1637-1655","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Early\u2010life stress and amyloidosis in mice share pathogenic pathways involving synaptic mitochondria and lipid metabolism"],"prefix":"10.1002","volume":"20","author":[{"given":"Janssen M.","family":"Kotah","sequence":"first","affiliation":[{"name":"Brain Plasticity Group Swammerdam Institute for Life Sciences \u2013 Center for Neuroscience University of Amsterdam  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mandy S. 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