{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T07:09:57Z","timestamp":1779174597359,"version":"3.51.4"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T00:00:00Z","timestamp":1779062400000},"content-version":"vor","delay-in-days":137,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>\n                    NOD\u2010like receptor protein 3 (NLRP3) inflammasome\u2010driven neuroinflammation contributes to Alzheimer\u2019s disease (AD) progression, yet effective strategies to target this pathway are limited. We investigated whether aerobic exercise performed in a fasted state, rather than the fed state, would potentiate \u03b2\u2010hydroxybutyrate (BHB)\u2010dependent inhibition of NLRP3 inflammasome signaling. Twenty\u2010month\u2010old male Wistar rats were randomly assigned to five groups: AD, AD\u2009+\u2009intermittent fasting (ADIF), AD\u2009+\u2009aerobic exercise (ADAE), ADIF\u2009+\u2009aerobic exercise (ADIFAE), and sham\u2010injected control (SC). AD\u2010like pathology was induced by bilateral intrahippocampal injection of amyloid\u2010\u03b2 (A\u03b2)\n                    <jats:sub>1\u201342<\/jats:sub>\n                    . The IF regimen consisted of a daily 14\u2010h fast (06:00\u201320:00). Exercise consisted of moderate\u2010intensity treadmill running (5 days\/week for 4 weeks), either in the fed state or after \u223c12.5\u2009h of fasting. A\u03b2 injection impaired spatial learning and memory, elevated soluble A\u03b2\n                    <jats:sub>1\u201342<\/jats:sub>\n                    (sA\u03b2), malondialdehyde (MDA), NF\u2010\u03baB, NLRP3, caspase\u20101, interleukin\u20101\u03b2 (IL\u20101\u03b2), and IL\u201018, and reduced superoxide dismutase (SOD) activity and brain\u2010derived neurotrophic factor (BDNF) expression in the hippocampus (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009 &lt; 0.05). Both IF and exercise partially reversed cognitive impairments by reducing sA\u03b2 and oxidative stress, increasing BHB, suppressing NF\u2010\u03baB\/NLRP3 signaling, and restoring BDNF (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009 &lt; 0.05), while fasted\u2010state exercise produced significantly larger effects than either intervention alone (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009 &lt; 0.05). Our findings suggest that performing exercise in a fasted state provides complementary metabolic, anti\u2010inflammatory, and cognitive benefits that exceed those of either intervention alone. This combined regimen may represent a promising nonpharmacological strategy for targeting metabolic\u2010immune and neurotrophic pathways relevant to AD progression.\n                  <\/jats:p>","DOI":"10.1155\/omcl\/9921337","type":"journal-article","created":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T06:20:31Z","timestamp":1779171631000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Intermittent Fasting Potentiates Aerobic Exercise to Reduce Hippocampal Amyloid Burden and Oxidative Stress via Suppression of NF\u2010\u03baB\/NLRP3 Signaling in an A\u03b2\u2010Injected Rat 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