{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T10:31:43Z","timestamp":1791973903642,"version":"4.4.0"},"reference-count":220,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2025,3,25]],"date-time":"2025-03-25T00:00:00Z","timestamp":1742860800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:p>\n                    Complex genetic relationships between neurodegenerative disorders and neuropsychiatric symptoms have been shown, suggesting shared pathogenic mechanisms and emphasizing the potential for developing common therapeutic targets. Apolipoprotein E (\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    ) genotypes and their corresponding protein (ApoE) isoforms may influence the biophysical properties of the cell membrane lipid bilayer. However, the role of\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    in central nervous system pathophysiology extended beyond its lipid transport function. In the present review article, we analyzed the links existing between\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    genotypes and the neurobiology of neuropsychiatric symptoms in neurodegenerative and vascular diseases.\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    genotypes (\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b52,\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b53, and\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54) were implicated in common mechanisms underlying a wide spectrum of neurodegenerative diseases, including sporadic Alzheimer\u2019s disease, synucleinopathies such as Parkinson\u2019s disease and Lewy body disease, stroke, and traumatic brain injury. These shared pathways often involved neuroinflammation, abnormal protein accumulation, or responses to acute detrimental events. Across these conditions,\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    variants are believed to contribute to the modulation of inflammatory responses, the regulation of amyloid and tau pathology, as well as the clearance of proteins such as \u03b1-synuclein. The bidirectional interactions among ApoE, amyloid and mitochondrial metabolism, immunomodulatory effects, neuronal repair, and remodeling underscored the complexity of ApoE\u2019s role in neuropsychiatric symptoms associated with these conditions since from early phases of cognitive impairment such as mild cognitive impairment and mild behavioral impairment. Besides ApoE-specific isoforms\u2019 link to increased neuropsychiatric symptoms in Alzheimer\u2019s disease (depression, psychosis, aberrant motor behaviors, and anxiety, not apathy), the\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54 genotype was also considered a significant genetic risk factor for Lewy body disease and its worse cognitive outcomes. Conversely, the\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b52 variant has been observed not to exert a protective effect equally in all neurodegenerative diseases. Specifically, in Lewy body disease, this variant may delay disease onset, paralleling its protective role in Alzheimer\u2019s disease, although its role in frontotemporal dementia is uncertain. The\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54 genotype has been associated with adverse cognitive outcomes across other various neurodegenerative conditions. In Parkinson\u2019s disease, the\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54 allele significantly impacted cognitive performance, increasing the risk of developing dementia, even in cases of pure synucleinopathies with minimal co-pathology from Alzheimer\u2019s disease. Similarly, in traumatic brain injury, recovery rates varied, with\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54 carriers demonstrating a greater risk of poor long-term cognitive outcomes and elevated levels of neuropsychiatric symptoms. Furthermore,\n                    <jats:italic toggle=\"yes\">APOE<\/jats:italic>\n                    \u03b54 influenced the age of onset and severity of stroke, as well as the likelihood of developing stroke-associated dementia, potentially due to its role in compromising endothelial integrity and promoting blood\u2013brain barrier dysfunction.\n                  <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-01274","type":"journal-article","created":{"date-parts":[[2025,3,30]],"date-time":"2025-03-30T09:10:13Z","timestamp":1743325813000},"page":"1528-1541","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":11,"title":["Neuropsychiatric symptoms and apolipoprotein E genotypes in neurocognitive disorders"],"prefix":"10.4103","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1674-9724","authenticated-orcid":false,"given":"Madia","family":"Lozupone","sequence":"first","affiliation":[{"name":"Department of Translational Biomedicine and Neuroscience \u201cDiBraiN\u201d, University of Bari Aldo Moro, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivana","family":"Leccisotti","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anita","family":"Mollica","sequence":"additional","affiliation":[{"name":"Department of Mental Health, ASL Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giuseppe","family":"Berardino","sequence":"additional","affiliation":[{"name":"Department of Mental Health, ASL Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Claudia","family":"Moretti","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario","family":"Altamura","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonello","family":"Bellomo","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio","family":"Daniele","sequence":"additional","affiliation":[{"name":"Neurology Unit, IRCCS Fondazione Policlinico Universitario A. Gemelli, Rome, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vittorio","family":"Dibello","sequence":"additional","affiliation":[{"name":"Department of Orofacial Pain and Dysfunction, Academic Center for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije Universiteit Amsterdam, Amsterdam, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincenzo","family":"Solfrizzi","sequence":"additional","affiliation":[{"name":"Department of Interdisciplinary Medicine, \u201cCesare Frugoni\u201d Internal and Geriatric Medicine and Memory Unit, University of Bari Aldo Moro, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emanuela","family":"Resta","sequence":"additional","affiliation":[{"name":"Translational Medicine and Health System Management, Department of Economy, University of Foggia, Foggia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco","family":"Panza","sequence":"additional","affiliation":[{"name":"Department of Interdisciplinary Medicine, \u201cCesare Frugoni\u201d Internal and Geriatric Medicine and Memory Unit, University of Bari Aldo Moro, Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,3,25]]},"reference":[{"key":"R1-20260421","first-page":"267","article-title":"Defective cholesterol metabolism in amyotrophic lateral sclerosis","volume":"58","author":"Abdel-Khalik","year":"2017","journal-title":"J Lipid Res"},{"key":"R2-20260421","first-page":"451","article-title":"Rapid amyloid-\u03b2 oligomer and protofibril accumulation in traumatic brain injury","volume":"28","author":"Abu Hamdeh","year":"2018","journal-title":"Brain Pathol"},{"key":"R3-20260421","first-page":"493","article-title":"Classification of stroke 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