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During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurodegeneration in the EC and hippocampus during AD has been clearly linked to impairments in memory and cognitive function, and a growing body of evidence indicates that molecular and functional neurodegeneration within the EC may play a primary role in cognitive decline in the early phases of AD. Defining the mechanisms underlying molecular neurodegeneration in the EC is crucial to determining its contributions to the pathogenesis of AD. Surprisingly few studies have focused on understanding the mechanisms of molecular neurodegeneration and selective vulnerability within the EC. However, there have been advancements indicating that early dysregulation of cellular and molecular signaling pathways in the EC involve neurodegenerative cascades including oxidative stress, neuroinflammation, glia activation, stress kinases activation, and neuronal loss. Dysfunction within the EC can impact the function of the hippocampus, which relies on entorhinal inputs, and further degeneration within the hippocampus can compound this effect, leading to severe cognitive disruption. This review assesses the molecular and cellular mechanisms underlying early degeneration in the EC during AD. These mechanisms may underlie the selective vulnerability of neuronal subpopulations in this brain region to the disease development and contribute both directly and indirectly to cognitive loss.<\/jats:p>\n               <jats:p>This paper has an associated Future Leader to Watch interview with the first author of the article.<\/jats:p>","DOI":"10.1242\/bio.056796","type":"journal-article","created":{"date-parts":[[2021,1,25]],"date-time":"2021-01-25T14:08:32Z","timestamp":1611583712000},"source":"Crossref","is-referenced-by-count":74,"title":["Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease"],"prefix":"10.1242","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9259-2837","authenticated-orcid":false,"given":"Olayemi Joseph","family":"Olajide","sequence":"first","affiliation":[{"name":"Division of Neurobiology, Department of Anatomy, University of Ilorin, Ilorin, Nigeria, PMB 1515"},{"name":"Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montr\u00e9al, Qu\u00e9bec, CanadaH4B 1R6"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcus E.","family":"Suvanto","sequence":"additional","affiliation":[{"name":"Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montr\u00e9al, Qu\u00e9bec, CanadaH4B 1R6"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1876-0898","authenticated-orcid":false,"given":"Clifton Andrew","family":"Chapman","sequence":"additional","affiliation":[{"name":"Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montr\u00e9al, Qu\u00e9bec, CanadaH4B 1R6"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2021,1,25]]},"reference":[{"key":"2021042701060719600_BIO056796C1","doi-asserted-by":"publisher","first-page":"95","DOI":"10.1016\/j.mad.2016.05.005","article-title":"Molecular pathophysiology of impaired glucose metabolism, mitochondrial dysfunction, and oxidative DNA damage in Alzheimer's disease brain","volume":"161","author":"Abolhassani","year":"2017","journal-title":"Mech. 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