{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T20:12:54Z","timestamp":1785269574886,"version":"3.55.0"},"reference-count":61,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2020,10,25]],"date-time":"2020-10-25T00:00:00Z","timestamp":1603584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Hypoglycaemia in diabetes (T2D) may increase the risk of Alzheimer's disease (AD). We hypothesized that hypoglycaemia\u2010induced amyloid\u2010related protein changes would be exacerbated in T2D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>A prospective, parallel study in T2D (n = 23) and controls (n = 23). Subjects underwent insulin\u2010induced hypoglycaemia with blood sampling at baseline, hypoglycaemia and post\u2010hypoglycaemia; proteomic analysis of amyloid\u2010related proteins was undertaken.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At baseline, amyloid\u2010precursor protein (APP) (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.01) was elevated and alpha\u2010synuclein (SNCA) (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.01) reduced in T2D. At hypoglycaemia, amyloid P\u2010component (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.01) was elevated and SNCA (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.05) reduced in T2D; APP (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.01) and noggin (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.05) were elevated and SNCA (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u2009.01) reduced in controls. In the post\u2010hypoglycaemia follow\u2010up period, APP and microtubule\u2010associated protein tau normalized in controls but showed a below\u2010baseline decrease in T2D; noggin normalized in both; SNCA normalized in T2D, with a below\u2010baseline decrease in controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The AD\u2010associated protein pattern found in T2D, with basal elevated APP and reduced SNCA, was exaggerated by hypoglycaemia with increased APP and decreased SNCA. Additional AD\u2010associated protein levels that changed in response to hypoglycaemia, particularly in T2D, included amyloid P\u2010component, microtubule\u2010associated protein tau, apolipoproteins A1 and E3, pappalysin and noggin. These results are in accordance with the reported detrimental effects of hypoglycaemia.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.14220","type":"journal-article","created":{"date-parts":[[2020,10,7]],"date-time":"2020-10-07T11:17:55Z","timestamp":1602069475000},"page":"338-349","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Hypoglycaemia in type\n                    <scp>2<\/scp>\n                    diabetes exacerbates amyloid\u2010related proteins associated with dementia"],"prefix":"10.1111","volume":"23","author":[{"given":"Abu Saleh Md","family":"Moin","sequence":"first","affiliation":[{"name":"Diabetes Research Center (DRC), Qatar Biomedical Research Institute (QBRI) Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF)  Doha 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