{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:35:41Z","timestamp":1792787741944,"version":"4.5.0"},"reference-count":29,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T00:00:00Z","timestamp":1776729600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Institute of Information and Communications Technology Planning and Evaluation","award":["RS-2023-00227929"],"award-info":[{"award-number":["RS-2023-00227929"]}],"id":[{"id":"https:\/\/ror.org\/01g0hqq23","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Amyloid-\u03b2 accumulation and misfolding are key features of Alzheimer's disease (AD), contributing to synaptic dysfunction, neuroinflammation, and neuronal loss. Normally, amyloid-\u03b2 is cleared by chaperone-assisted folding, enzymes such as neprilysin and insulin-degrading enzyme, and autophagy pathways. In AD, these mechanisms become impaired, leading to toxic aggregation. Enhancing the activity of endogenous degrading enzymes offers a promising therapeutic approach, with electromagnetic (EM) fields emerging as a potential noninvasive method to promote amyloid-\u03b2 clearance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study computationally evaluates whether controlled EM wave exposure (100\u2013900\u2005MHz) delivered through a waveguide can enhance amyloid-\u03b2 degradation by accelerating enzyme activation and reducing Gibbs free energy barriers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A mechanistic model linking EM stimulation with cellular stress responses, chaperone activity, enzyme delivery, and autophagy was developed. Quantum-chemical simulations evaluated changes in Gibbs free energy and reaction rates under no EM field, low-intensity EM (1.0\u2009\u00d7\u200910\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      a.u.), and optimized EM intensity (5.09\u2009\u00d7\u200910\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      <jats:sup>0<\/jats:sup>\n                      a.u.).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Computational simulations revealed that EM stimulation enhances enzymatic activation by lowering the Gibbs free energy barrier. Without an electric field, \u0394G was 66.00\u2005kJ\u00b7mol\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      with a reaction rate of 56.5\u2005s\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      . Low-intensity EM slightly reduced \u0394G to 65.87\u2005kJ\u00b7mol\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      and increased the rate to 67.5\u2005s\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      . At optimized EM intensity, \u0394G decreased to 52.10\u2005kJ\u00b7mol\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      , raising the reaction rate to 1.18\u2009\u00d7\u200910\n                      <jats:sup>4<\/jats:sup>\n                      s\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      , indicating significantly accelerated enzyme activity and improved amyloid-\u03b2 degradation potential.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The integrated model shows that optimized EM stimulation enhances enzyme-mediated amyloid-\u03b2 degradation by lowering energy barriers and increasing reaction rates, supporting a potential noninvasive therapeutic strategy for AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877261444315","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T14:02:36Z","timestamp":1776780156000},"page":"1742-1750","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Electromagnetic field induced activation of amyloid-\u03b2 degrading enzyme, neprilysin, for accelerated Alzheimer's disease therapy"],"prefix":"10.1177","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8705-1473","authenticated-orcid":false,"given":"Sohom","family":"Bhattacharjee","sequence":"first","affiliation":[{"name":"Korea Aerospace University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeeln","family":"Choi","sequence":"additional","affiliation":[{"name":"CHA University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moon Que","family":"Lee","sequence":"additional","affiliation":[{"name":"University of Seoul"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MinYoung","family":"Kim","sequence":"additional","affiliation":[{"name":"CHA University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yash Hemant","family":"Shah","sequence":"additional","affiliation":[{"name":"Korea Aerospace University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdul","family":"Hadee","sequence":"additional","affiliation":[{"name":"Korea Aerospace University"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Choon Sik","family":"Cho","sequence":"additional","affiliation":[{"name":"Korea Aerospace University"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,4,21]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1159\/000097371"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41572-021-00269-y"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41380-024-02509-5"},{"key":"e_1_3_3_5_2","first-page":"500","article-title":"Turning on lights to stop neurodegeneration: the potential of near infrared light therapy in Alzheimer\u2019s and Parkinson\u2019s disease","volume":"10","author":"Johnstone DM","year":"2016","unstructured":"Johnstone DM, Moro C, Stone J, et al. 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