{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T22:42:24Z","timestamp":1791931344131,"version":"4.3.4"},"reference-count":341,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2022,6,6]],"date-time":"2022-06-06T00:00:00Z","timestamp":1654473600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000320","name":"Alzheimer's Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000320","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The\n                    <jats:italic>APOE<\/jats:italic>\n                    gene encoding the Apolipoprotein E protein is the single most significant genetic risk factor for late\u2010onset Alzheimer's disease. The\n                    <jats:italic>APOE4<\/jats:italic>\n                    genotype confers a significantly increased risk relative to the other two common genotypes\n                    <jats:italic>APOE3<\/jats:italic>\n                    and\n                    <jats:italic>APOE2<\/jats:italic>\n                    . Intriguingly,\n                    <jats:italic>APOE4<\/jats:italic>\n                    has been associated with neuropathological and cognitive deficits in the absence of Alzheimer's disease\u2010related amyloid or tau pathology. Here, we review the extensive literature surrounding the impact of\n                    <jats:italic>APOE<\/jats:italic>\n                    genotype on central nervous system dysfunction, focussing on preclinical model systems and comparison of\n                    <jats:italic>APOE3<\/jats:italic>\n                    and\n                    <jats:italic>APOE4<\/jats:italic>\n                    , given the low global prevalence of\n                    <jats:italic>APOE2<\/jats:italic>\n                    . A multi\u2010hit hypothesis is proposed to explain how\n                    <jats:italic>APOE4<\/jats:italic>\n                    shifts cerebral physiology towards pathophysiology through interconnected hits. These hits include the following: neurodegeneration, neurovascular dysfunction, neuroinflammation, oxidative stress, endosomal trafficking impairments, lipid and cellular metabolism disruption, impaired calcium homeostasis and altered transcriptional regulation. The hits, individually and in combination, leave the\n                    <jats:italic>APOE4<\/jats:italic>\n                    brain in a vulnerable state where further cumulative insults will exacerbate degeneration and lead to cognitive deficits in the absence of Alzheimer's disease pathology and also a state in which such pathology may more easily take hold. We conclude that current evidence supports an\n                    <jats:italic>APOE4<\/jats:italic>\n                    multi\u2010hit hypothesis, which contributes to an\n                    <jats:italic>APOE4<\/jats:italic>\n                    pathophysiological state. We highlight key areas where further study is required to elucidate the complex interplay between these individual mechanisms and downstream consequences, helping to frame the current landscape of existing\n                    <jats:italic>APOE<\/jats:italic>\n                    \u2010centric literature.\n                  <\/jats:p>","DOI":"10.1111\/ejn.15685","type":"journal-article","created":{"date-parts":[[2022,5,5]],"date-time":"2022-05-05T04:34:21Z","timestamp":1651725261000},"page":"5476-5515","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["A multi\u2010hit hypothesis for an\n                    <i>APOE4<\/i>\n                    \u2010dependent pathophysiological state"],"prefix":"10.1111","volume":"56","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4789-9773","authenticated-orcid":false,"given":"Oliver George","family":"Steele","sequence":"first","affiliation":[{"name":"School of Life Sciences 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