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Since the cellular mechanisms governing this relationship are poorly understood, we explored whether ATP-sensitive potassium (K\n                    <jats:sub>ATP<\/jats:sub>\n                    ) channels, which couple changes in energy availability with cellular excitability, play a role in AD pathogenesis. First, we demonstrate that K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel subunits Kir6.2\/\n                    <jats:italic>KCNJ11<\/jats:italic>\n                    and SUR1\/\n                    <jats:italic>ABCC8<\/jats:italic>\n                    were expressed on excitatory and inhibitory neurons in the human brain, and cortical expression of\n                    <jats:italic>KCNJ11<\/jats:italic>\n                    and\n                    <jats:italic>ABCC8<\/jats:italic>\n                    changed with AD pathology in humans and mice. Next, we explored whether eliminating neuronal K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel activity uncoupled the relationship between metabolism, excitability, and A\u03b2 pathology in a potentially novel mouse model of cerebral amyloidosis and neuronal K\n                    <jats:sub>ATP<\/jats:sub>\n                    channel ablation (i.e., amyloid precursor protein [APP]\/PS1 Kir6.2\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mouse). Using both acute and chronic paradigms, we demonstrate that Kir6.2-K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels are metabolic sensors that regulate hyperglycemia-dependent increases in interstitial fluid levels of A\u03b2, amyloidogenic processing of APP, and amyloid plaque formation, which may be dependent on lactate release. These studies identify a potentially new role for Kir6.2-K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels in AD and suggest that pharmacological manipulation of Kir6.2-K\n                    <jats:sub>ATP<\/jats:sub>\n                    channels holds therapeutic promise in reducing A\u03b2 pathology in patients with diabetes or prediabetes.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.162454","type":"journal-article","created":{"date-parts":[[2023,5,2]],"date-time":"2023-05-02T19:50:38Z","timestamp":1683057038000},"source":"Crossref","is-referenced-by-count":30,"title":["KATP channels are necessary for glucose-dependent increases in amyloid-\u03b2 and Alzheimer\u2019s disease\u2013related pathology"],"prefix":"10.1172","volume":"8","author":[{"given":"John","family":"Grizzanti","sequence":"first","affiliation":[{"name":"Department of Physiology and Pharmacology and"},{"name":"Department of Internal Medicine, Wake Forest School of Medicine, 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USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0048-3738","authenticated-orcid":true,"given":"Sarah D.","family":"Kaye","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology and"},{"name":"Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1572-7360","authenticated-orcid":true,"given":"Caitlin M.","family":"Carroll","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology and"},{"name":"Department of Internal Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1430-493X","authenticated-orcid":true,"given":"Nicholas J.","family":"Constantino","sequence":"additional","affiliation":[{"name":"Department of 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