{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T02:03:00Z","timestamp":1771639380695,"version":"3.50.1"},"reference-count":46,"publisher":"Bentham Science Publishers Ltd.","issue":"10","content-domain":{"domain":["eurekaselect.com"],"crossmark-restriction":true},"short-container-title":["CAR"],"published-print":{"date-parts":[[2021,1,15]]},"abstract":"<jats:sec>\n<jats:title>Objective:<\/jats:title>\n<jats:p>Alzheimer's disease (AD) is one of the worst neurodegenerative disorders\nworldwide, with extracellular senile plaques (SP), subsequent intracellular neurofibrillary tangles\n(NFTs) and final neuron loss and synaptic dysfunction as the main pathological characteristics. Excessive\napoptosis is the main cause of irreversible neuron loss. Thus, therapeutic intervention for these\npathological features has been considered a promising strategy to treat or prevent AD. Dihydroartemisin\n(DHA) is a widely used first-line drug for malaria. Our previous study showed that DHA treatment\nsignificantly accelerated A\u03b2 clearance, improved memory and cognitive deficits in vivo and restored\nautophagic flux both in vivo and in vitro.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Methods:<\/jats:title>\n<jats:p>The present study intended to explore the neuroprotective effect of DHA on neuron loss in\nAPP\/PS1 double-transgenic mice and the underlying mechanisms involved. Transmission electron\nmicroscope (TEM) analysis showed that DHA significantly reduced the swollen endoplasmic reticulum\n(ER) in APP\/PS1 mice. Western blot analysis indicated that DHA upregulated the level of NeuN,\nNeuroD, MAP2, and synaptophysin and promoted neurite outgrowth. Meanwhile, DHA greatly corrected\nthe abnormal levels of Brain-derived neurotrophic factor (BDNF) and rescued the neuronal loss\nin the hippocampal CA1 area. Western blot analysis revealed that DHA notably down-regulated the\nprotein expression of full length caspase-3, cleaved caspase-3 and Bax. In parallel, the expression of\nthe anti-apoptotic protein Bcl-2 increased after oral DHA treatment.<\/jats:p>\n<\/jats:sec>\n<jats:sec>\n<jats:title>Results:<\/jats:title>\n<jats:p>Altogether, these results indicate that DHA protected AD mice from neuron loss via promoting\nthe expression of BDNF and other neuroplasticity-associated proteins and suppressing the inhibition\nof neuronal apoptosis.<\/jats:p>\n<\/jats:sec>","DOI":"10.2174\/1567205017666201215124746","type":"journal-article","created":{"date-parts":[[2021,1,4]],"date-time":"2021-01-04T15:07:57Z","timestamp":1609772877000},"page":"916-925","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Dihydroartemisinin Ameliorates Decreased Neuroplasticity-Associated Proteins and Excessive Neuronal Apoptosis in APP\/PS1 Mice"],"prefix":"10.2174","volume":"17","author":[{"given":"Yueyang","family":"Zhao","sequence":"first","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhimin","family":"Long","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuanjie","family":"Liu","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Min","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Pathology, Suining Municipal Hospital of TCM, Suining City, Si Chuan Province, 629000, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yu","family":"Qiu","sequence":"additional","affiliation":[{"name":"Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, College of Stomatology, Chongqing Medical University, Chongqing, 401147, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nur F.B.","family":"Idris","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aijia","family":"Song","sequence":"additional","affiliation":[{"name":"Laboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kejian","family":"Wang","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guiqiong","family":"He","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center, Chongqing Medical University, Chongqing, 400016, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","first-page":"465","DOI":"10.1016\/j.tibs.2006.06.006","volume":"31","author":"Barnham K.J.","year":"2006","unstructured":"Barnham K.J.; Cappai R.; Beyreuther K.; Masters C.L.; Hill A.F.; Delineating common molecular mechanisms in Alzheimer\u2019s and prion diseases. 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