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However, the precise involvement is not well understood, and it remains unclear exactly how such dysregulated lipid metabolism and altered nutrient status, especially changes in phosphatidylcholine, B12, and folate, are connected to the hallmark pathology in AD (i.e., amyloidogenesis).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We have postulated that genetic susceptibility (i.e., APOE \u03b54\/\u03b54) to environmental exposure to emissions of nitrous oxide (N\n                      <jats:sub>2<\/jats:sub>\n                      O) could underlie the onset of AD and its early neuropsychiatric correlates\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and Discussion<\/jats:title>\n                    <jats:p>The current theoretical editorial describes, using clinical, preclinical, and in\u2009vitro evidences, how this model contributes not only to amyloidogenesis but also other nonopioid effects, specifically altered lipid metabolism, depletion of vitamin B12, and disruption of the folate\u2010mediated one carbon metabolic pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.trci.2019.03.002","type":"journal-article","created":{"date-parts":[[2019,4,29]],"date-time":"2019-04-29T21:28:55Z","timestamp":1556573335000},"page":"139-145","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["A model of lipid dysregulation and altered nutrient status in Alzheimer's disease"],"prefix":"10.1002","volume":"5","author":[{"given":"Keith","family":"Fluegge","sequence":"first","affiliation":[{"name":"Institute of Health and Environmental Research Columbus OH 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