{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:23:05Z","timestamp":1787026985161,"version":"build-2736575974"},"reference-count":71,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Postgraduate Research & Practice Innovation Program of Harbin Medical University","award":["YJSCX2024-45HYD"],"award-info":[{"award-number":["YJSCX2024-45HYD"]}]},{"name":"First-Class Disciplines and Specialties Project of the Second Affiliated Hospital of Harbin Medical University","award":["YLXK202007"],"award-info":[{"award-number":["YLXK202007"]}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Neurosci."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Alzheimer\u2019s disease (AD) is the most prevalent neurodegenerative disorder. Emerging evidence indicates that fatty acid oxidation is impaired in both patients with AD and AD animal models. In the brain, fatty acid metabolism occurs predominantly in astrocytes. Diets enriched in monounsaturated fatty acids (MUFAs) are often recommended for individuals with AD. Oleic acid (OA), a common dietary MUFA, has been shown to reduce amyloid plaque accumulation in transgenic mouse models of AD. Moreover, OA decreases the expression of acetyl-CoA carboxylase beta (ACACB\/ACC2), a key regulator of fatty acid \u03b2-oxidation. However, the precise mechanism by which OA may alleviate amyloid plaque deposition through modulation of brain fatty acid metabolism remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To determine whether dietary OA supplementation partially restores astrocytic fatty acid metabolism by suppressing ACACB and enhancing fatty acid \u03b2-oxidation, thereby attenuating AD-related pathology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using NHANES 2011\u20132014 data, we applied survey-weighted multivariable logistic regression to examine the association between energy-adjusted MUFA intake and low cognitive function, with adjustment for multiple testing. We then screened GEO datasets to identify AD-associated genes involved in fatty acid metabolic dysregulation, identifying ACACB as a candidate target. The expression of ACACB and its downstream effector carnitine palmitoyltransferase 1A (CPT1A) were validated in mouse and cell models. APP\/PS1 mice received dietary OA supplementation, followed by behavioral testing and brain histopathological analyses. In parallel, an A\u03b21\u201342-induced astrocyte injury model was used to assess lipid droplet accumulation, mitochondrial function, and cellular energy metabolism. ACACB knockdown\/overexpression and CPT1A overexpression were used to test pathway-specific effects of OA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Higher MUFA intake was associated with better cognitive function. ACACB as a key fatty acid metabolism-related gene in AD. In APP\/PS1 mice, OA improved cognitive performance and reduced A\u03b2 plaque deposition, accompanied by decreased ACACB and increased CPT1A expression in brain tissue.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , OA modulated ACC2 activity through protein kinase A (PKA) signaling, increased fatty acid \u03b2-oxidation, reduced lipid droplet accumulation, restored mitochondrial membrane potential and ATP production, and enhanced astrocyte-mediated support of neuronal synaptic growth.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>OA ameliorates AD-related pathology and cognitive impairment by restoring astrocytic fatty acid \u03b2-oxidation through the PKA\/ACACB\/CPT1A pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fnins.2026.1771310","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T05:44:43Z","timestamp":1776231883000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Oleic acid improves pathological changes in A\u03b21\u201342-induced astrocytes and Alzheimer\u2019s disease mouse models through PKA\/ACACB\/CPT1A"],"prefix":"10.3389","volume":"20","author":[{"given":"YiBo","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Neurology, Second Affiliated Hospital of Harbin Medical University","place":["Harbin, Heilongjiang, China"]},{"name":"Department of Biochemistry and Molecular Biology, School of Basic Medicine, Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianan","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Neurology, Second Affiliated Hospital of Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Neurology, Second Affiliated Hospital of Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yahui","family":"Peng","sequence":"additional","affiliation":[{"name":"Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mingjie","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Neurology, Second Affiliated Hospital of Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Neurology, Second Affiliated Hospital of Harbin Medical University","place":["Harbin, Heilongjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,4,15]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"410","DOI":"10.1038\/nature11059","article-title":"Astrocyte glypicans 4 and 6 promote formation of excitatory synapses via GluA1 AMPA receptors","volume":"486","author":"Allen","year":"2012","journal-title":"Nature"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"1598","DOI":"10.1002\/alz.13016","article-title":"Alzheimer\u2019s disease facts and figures","volume":"19","year":"2023","journal-title":"Alzheimers Dement."},{"key":"ref3","doi-asserted-by":"publisher","first-page":"3708","DOI":"10.1002\/alz.13809","article-title":"Alzheimer\u2019s disease facts and figures","volume":"20","year":"2024","journal-title":"Alzheimers Dement."},{"key":"ref4","doi-asserted-by":"publisher","first-page":"321","DOI":"10.1111\/j.1750-3639.2010.00449.x","article-title":"Oleic acid ameliorates amyloidosis in cellular and mouse models of Alzheimer\u2019s disease","volume":"21","author":"Amtul","year":"2011","journal-title":"Brain Pathol."},{"key":"ref5","doi-asserted-by":"publisher","first-page":"683459","DOI":"10.3389\/fcell.2021.683459","article-title":"The ageing brain: molecular and cellular basis of neurodegeneration","volume":"9","author":"Azam","year":"2021","journal-title":"Front. 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