{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T14:13:12Z","timestamp":1780063992317,"version":"3.54.0"},"reference-count":31,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T00:00:00Z","timestamp":1780012800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Aging Neurosci."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Alzheimer\u2019s disease (AD) is a major neurodegenerative disorder characterized by amyloid-\u03b2 (A\u03b2) accumulation, neurofibrillary tangles, and progressive cognitive decline. Despite significant advances in understanding its pathophysiology, current therapeutic options provide limited symptomatic relief. The present study investigated the nootropic and anti-amnesic effects of propranolol (PRO) in a scopolamine (SCP)-induced AD-like rat model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Wistar rats received PRO (10, 30, or 50 mg\/kg, p.o.) or donepezil (DPZ; 1 mg\/kg) for 17 days. Cognitive deficits were induced by SCP (1 mg\/kg, i.p.) administration from day 9 onward. Behavioral performance was assessed using the Novel Object Recognition (NOR) and Elevated Plus Maze (EPM) tests. Molecular and cellular analyses were conducted to evaluate synaptic plasticity markers (CaMKII, CREB, BDNF, PKM\u03b6), mitochondrial function, oxidative stress parameters, and inflammatory markers (GFAP, TNF-\u03b1).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Propranolol treatment significantly improved long-term memory performance, enhanced recognition index, and attenuated anxiety-like behavior in SCP-treated rats. These behavioral effects were associated with upregulation of CaMKII\u2013CREB\u2013BDNF\u2013PKM\u03b6 signaling, improvement in mitochondrial membrane potential (\u0394\u03c8m), reduction in reactive oxygen species (ROS) generation and A\u03b21\u201342 accumulation, and decreased expression of GFAP and TNF-\u03b1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The findings suggest that propranolol mitigates SCP-induced cognitive impairments, potentially through modulation of synaptic plasticity\u2013 related signaling, mitochondrial function, and neuroinflammatory responses. These results indicate the therapeutic potential of propranolol in experimental models of AD-related neurodegeneration, warranting further investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fnagi.2026.1729046","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T06:10:17Z","timestamp":1780035017000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Propranolol reinstates mitochondrial dynamics and synaptic memory pathways through CaMKII\/CREB\u2013BDNF\/ PKM\u03b6 cascades in an AD-like rat model"],"prefix":"10.3389","volume":"18","author":[{"family":"Pinky","sequence":"first","affiliation":[{"name":"Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"family":"Neha","sequence":"additional","affiliation":[{"name":"Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Medha","family":"Kaushik","sequence":"additional","affiliation":[{"name":"Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prachi","family":"Tiwari","sequence":"additional","affiliation":[{"name":"Department of Paramedical Sciences, School of Rehabilitation Health Sciences, Jamia Hamdard","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"El-Tanani","sequence":"additional","affiliation":[{"name":"RAK College of Pharmacy, RAK Medical and Health Sciences University","place":["Ras Al Khaimah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Syed Arman","family":"Rabbani","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacy and Pharmacology, RAK College of Pharmacy, RAK Medical and Health Sciences University","place":["Ras Al Khaimah, United Arab Emirates"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suhel","family":"Parvez","sequence":"additional","affiliation":[{"name":"Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard","place":["New Delhi, India"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,29]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"256","DOI":"10.1016\/j.psyneuen.2006.12.013","article-title":"Cognitive impairment associated to HPA axis hyperactivity after maternal separation in rats.","volume":"32","author":"Aisa","year":"2007","journal-title":"Psychoneuroendocrinology"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1345","DOI":"10.3233\/JAD-170543","article-title":"Oxidative stress, amyloid-\u03b2 peptide, and altered key molecular pathways in the pathogenesis and progression of Alzheimer\u2019s disease.","volume":"62","author":"Allan Butterfield","year":"2018","journal-title":"J. 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