{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T10:50:28Z","timestamp":1772621428647,"version":"3.50.1"},"reference-count":68,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T00:00:00Z","timestamp":1772582400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Mol. Neurosci."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Apolipoprotein E (ApoE), reelin, and several other proteins bind ApoE-receptor 2 (apoER2), distinguished from other members of its receptor family by signal transduction which enhances the activity of N-methyl D-aspartate (NMDA) receptors. Evidence indicates that this signal transduction depends upon apoER2 forming dimers or other high-order clusters. It seems noteworthy therefore that protein products of major\n                      <jats:italic>APOE<\/jats:italic>\n                      gene variants differ in their numbers of cysteines capable of forming disulfide dimers, with the allele (\u03b54) associated with highest rates of Alzheimer\u2019s disease (AD) possessing none. Thus, lower AD risk may be associated with the ability of ApoE to dimerize and thereby promote apoER2 dimerization and signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We examined calcium fluxes via the NMDA receptor in neurons derived from the NTera2 cell line in response to conditioned medium from human astrocytes differing in\n                      <jats:italic>APOE<\/jats:italic>\n                      genotype, recombinant ApoE proteins, reelin, amyloid \u03b2-peptide (A\u03b2) preparations differing in their aggregation states, and secreted amyloid precursor protein (sAPP). Signaling through apoER2 was inhibited by receptor-associated protein (RAP) or siRNA directed against apoER2.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Reelin, fibrillar A\u03b2, ApoE3, and conditioned medium from\n                      <jats:italic>APOE<\/jats:italic>\n                      \u03b53 astrocytes elevated calcium fluxes, and this phenomenon required apoER2. By contrast, ApoE4 and oligomeric A\u03b2 antagonized activation. sAPP showed high-affinity binding to apoER2 and enhanced responses to reelin.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings suggest a comprehensive hypothesis for the pathogenesis of AD whereby the common factor in development of disease is antagonism of apoER2, likely to include agents that cannot promote the receptor\u2019s dimerization yet competitively inhibit those ligands that can cause dimerization.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fnmol.2026.1781541","type":"journal-article","created":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T05:43:18Z","timestamp":1772602998000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Modulation of apolipoprotein E receptor-2 by ApoE4, amyloid \u03b2-peptide, reelin, and secreted amyloid precursor protein: a common point of impact in Alzheimer\u2019s disease pathogenesis"],"prefix":"10.3389","volume":"19","author":[{"given":"Steven W.","family":"Barger","sequence":"first","affiliation":[{"name":"Department of Geriatrics, University of Arkansas for Medical Sciences","place":["Little Rock, AR, United States"]},{"name":"Department of Neuroscience, University of Arkansas for Medical Sciences","place":["Little Rock, AR, United States"]},{"name":"Geriatric Research Education and Clinical Center, Central Arkansas Veterans Healthcare System","place":["Little Rock, AR, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andr\u00e9a M.","family":"Moerman-Herzog","sequence":"additional","affiliation":[{"name":"Department of Geriatrics, University of Arkansas for Medical Sciences","place":["Little Rock, AR, United States"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,4]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"293","DOI":"10.1203\/PDR.0b013e3181cb8e68","article-title":"Apolipoprotein E4 and sex affect neurobehavioral performance in primary school children.","volume":"67","author":"Acevedo","year":"2010","journal-title":"Pediatr. 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