{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T12:08:38Z","timestamp":1782821318488,"version":"3.54.5"},"reference-count":122,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2024,2,24]],"date-time":"2024-02-24T00:00:00Z","timestamp":1708732800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2024,3,5]]},"abstract":"<jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Alzheimer\u2019s disease (AD) is characterized by disrupted proteostasis and macroautophagy (hereafter \u201cautophagy\u201d). The pharmacological agent suramin has known autophagy modulation properties with potential efficacy in mitigating AD neuronal pathology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>In the present work, we investigate the impact of forebrain neuron exposure to suramin on the Akt\/mTOR signaling pathway, a major regulator of autophagy, in comparison with rapamycin and chloroquine. We further investigate the effect of suramin on several AD-related biomarkers in sporadic AD (sAD)-derived forebrain neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Neurons differentiated from ReNcell neural progenitors were used to assess the impact of suramin on the Akt\/mTOR signaling pathway relative to the autophagy inducer rapamycin and autophagy inhibitor chloroquine. Mature forebrain neurons were differentiated from induced pluripotent stem cells (iPSCs) sourced from a late-onset sAD patient and treated with 100\u03bcM suramin for 72\u200ah, followed by assessments for amyloid-\u03b2, phosphorylated tau, oxidative\/nitrosative stress, and synaptic puncta density.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Suramin treatment of sAD-derived neurons partially ameliorated the increased p-Tau(S199)\/Tau ratio, and fully remediated the increased glutathione to oxidized nitric oxide ratio, observed in untreated sAD-derived neurons relative to healthy controls. These positive results may be due in part to the distinct increases in Akt\/mTOR pathway mediator p-p70S6K noted with suramin treatment of both ReNcell-derived and iPSC-derived neurons. Longer term neuronal markers, such as synaptic puncta density, were unaffected by suramin treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>These findings provide initial evidence supporting the potential of suramin to reduce the degree of dysregulation in sAD-derived forebrain neurons in part via the modulation of autophagy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-230600","type":"journal-article","created":{"date-parts":[[2024,2,27]],"date-time":"2024-02-27T10:57:50Z","timestamp":1709031470000},"page":"301-318","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Impact of Suramin on Key Pathological Features of Sporadic Alzheimer\u2019s Disease-Derived Forebrain Neurons"],"prefix":"10.1177","volume":"98","author":[{"given":"Robert A.","family":"Culibrk","sequence":"first","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine A.","family":"Ebbert","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Yeisley","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Chen","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatir A.","family":"Qureshi","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juergen","family":"Hahn","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariah S.","family":"Hahn","sequence":"additional","affiliation":[{"name":"Rensselaer Polytechnic Institute","place":["USA"]},{"name":"Rensselaer Polytechnic Institute","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2024,2,24]]},"reference":[{"key":"e_1_3_6_2_2","doi-asserted-by":"publisher","DOI":"10.2174\/0929867323666161213101126"},{"key":"e_1_3_6_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa2212948"},{"key":"e_1_3_6_4_2","doi-asserted-by":"publisher","DOI":"10.3389\/fnagi.2020.583884"},{"key":"e_1_3_6_5_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms22147475"},{"key":"e_1_3_6_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00688828"},{"key":"e_1_3_6_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-020-16984-1"},{"key":"e_1_3_6_8_2","doi-asserted-by":"publisher","DOI":"10.3390\/antiox10050694"},{"key":"e_1_3_6_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/cdd.2014.150"},{"key":"e_1_3_6_10_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0094496"},{"key":"e_1_3_6_11_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20051249"},{"key":"e_1_3_6_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbas.2022.100050"},{"key":"e_1_3_6_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pharmthera.2018.03.004"},{"key":"e_1_3_6_14_2","doi-asserted-by":"publisher","DOI":"10.1002\/cmdc.200700003"},{"key":"e_1_3_6_15_2","doi-asserted-by":"publisher","DOI":"10.1080\/15548627.2015.1009778"},{"key":"e_1_3_6_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2014.08.019"},{"key":"e_1_3_6_17_2","doi-asserted-by":"publisher","DOI":"10.1177\/0300060520927919"},{"key":"e_1_3_6_18_2","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2022.778479"},{"key":"e_1_3_6_19_2","doi-asserted-by":"publisher","DOI":"10.1186\/s13195-017-0317-z"},{"key":"e_1_3_6_20_2","first-page":"313","article-title":"Alteration of the Wnt\/GSK3\u03b2\/\u03b2-catenin signalling pathway by rapamycin ameliorates pathology in an Alzheimer\u2019s disease model","volume":"44","author":"Chen J","year":"2019","unstructured":"ChenJ, LongZ, LiY, LuoM, LuoS, HeG (2019) Alteration of the Wnt\/GSK3\u03b2\/\u03b2-catenin signalling pathway by rapamycin ameliorates pathology in an Alzheimer\u2019s disease model. 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