{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T19:41:35Z","timestamp":1787773295468,"version":"build-2784847793"},"reference-count":69,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"US-Food and Drug Administration"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer's Disease Reports"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>High-fat diet (HFD) consumption is linked to Alzheimer's disease (AD). Identifying changes in the mRNA expression due to the ingestion of HFD in the intestine\u2014often called the second brain due to its dense enteric neurons\u2014could offer insights into AD development and progression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Objective<\/jats:title>\n            <jats:p>This study assesses whether the introduction of HFD at adult-age influence expression of AD-related genes in the intestines of Wild-type (WT) or the amyloid precursor protein\/presenilin1 (APP\/PS1)-overexpressing Transgenic (TG) rats.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Twelve-month-old WT and TG rats (male and female) were fed a control diet (CD; 8% energy from fat), or HFD (45% energy from fat) for six months. Ileal tissues were assessed for the mRNA expression of genes responsible for development\/progression of AD.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>\n              The WT HFD-fed rats (compared to CD-fed rats) showed increased mRNA expression of genes involved in the development of AD. In contrast, the TG HFD-fed female group, showed a higher number of upregulated genes compared to their respective CD-fed TG group. In TG HFD-fed rats there was higher mRNA expression of genes crucial for synaptic transmission such as\n              <jats:italic>Brain-derived neurotrophic factor<\/jats:italic>\n              in females and\n              <jats:italic>Choline acetyltransferase<\/jats:italic>\n              in males. Expression of\n              <jats:italic>Plasminogen<\/jats:italic>\n              was higher in HFD-fed TG female rats and HFD-fed WT male rats. Overall, the HFD-fed WT male showed mRNA expression of genes involved in the development of AD. However, HFD-fed TG females were more vulnerable for the progression of AD. It is likely that the enteric\n              <jats:italic>Plasminogen<\/jats:italic>\n              plays a major role in gut-brain axis for the development of AD in WT male, and progression of AD in TG female during the consumption of HFD.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>The consumption of HFD perturbed the expression of enteric genes known to be involved in amyloid-\u03b2 generation, clearance, and degradation, in a sex-dependent manner.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1177\/25424823251358414","type":"journal-article","created":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T07:12:11Z","timestamp":1754982731000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":3,"title":["Potential link of high fat diet and mRNA expression of Alzheimer's disease-related genes in the enteric mucosa of a rat model of Alzheimer's disease"],"prefix":"10.1177","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4045-5993","authenticated-orcid":false,"given":"Kuppan","family":"Gokulan","sequence":"first","affiliation":[{"name":"Division of Microbiology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kumari","family":"Karn","sequence":"additional","affiliation":[{"name":"Division of Microbiology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6255-8809","authenticated-orcid":false,"given":"Sumit","family":"Sarkar","sequence":"additional","affiliation":[{"name":"Division of Neurotoxicology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-0561-2908","authenticated-orcid":false,"given":"James","family":"Raymick","sequence":"additional","affiliation":[{"name":"Division of Neurotoxicology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9496-6636","authenticated-orcid":false,"given":"Sangeeta","family":"Khare","sequence":"additional","affiliation":[{"name":"Division of Microbiology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,8,12]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2018.06.3063"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.4081\/cp.2017.987"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.3390\/antiox13121504"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10048-024-00791-7"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.3390\/cells10113164"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2015.05.016"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-016-1662-x"},{"key":"e_1_3_3_9_2","first-page":"339","article-title":"Relationship between lipid metabolism and plasma concentration of amyloid precursor protein and apolipoprotein E","volume":"2","author":"Boyt AA","year":"1999","unstructured":"Boyt AA, Taddei K, Hallmayer J, et al. 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