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Here, we utilized loss-of-function genetic mouse models to causally evaluate the role of\n                  <jats:sub>m<\/jats:sub>\n                  Ca\n                  <jats:sup>2+<\/jats:sup>\n                  uptake by conditionally deleting the mitochondrial calcium uniporter channel (mtCU) in a robust mouse model of AD. Loss of neuronal\n                  <jats:sub>m<\/jats:sub>\n                  Ca\n                  <jats:sup>2+<\/jats:sup>\n                  uptake reduced A\u03b2 and tau-pathology, synaptic dysfunction, and cognitive decline in 3xTg-AD mice. Knockdown of\n                  <jats:italic>Mcu<\/jats:italic>\n                  in an\n                  <jats:italic>in vitro<\/jats:italic>\n                  model of AD significantly reduced matrix Ca\n                  <jats:sup>2+<\/jats:sup>\n                  content, redox imbalance, and mitochondrial dysfunction. The preservation of mitochondrial function rescued the AD-dependent decline in autophagic capacity and protected neurons against amyloidosis and cell death. This was corroborated by\n                  <jats:italic>in vivo<\/jats:italic>\n                  data showing improved mitochondrial structure and apposition in AD mice with loss of neuronal\n                  <jats:italic>Mcu<\/jats:italic>\n                  . These results suggest that inhibition of neuronal\n                  <jats:sub>m<\/jats:sub>\n                  Ca\n                  <jats:sup>2+<\/jats:sup>\n                  uptake represents a powerful therapeutic target to impede AD progression.\n                <\/jats:p>","DOI":"10.1101\/2023.10.11.561889","type":"posted-content","created":{"date-parts":[[2023,10,16]],"date-time":"2023-10-16T13:00:22Z","timestamp":1697461222000},"source":"Crossref","is-referenced-by-count":7,"title":["Genetic ablation of neuronal mitochondrial calcium uptake impedes Alzheimer\u2019s disease progression"],"prefix":"10.64898","author":[{"given":"Pooja","family":"Jadiya","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Berezhnaya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devin W.","family":"Kolmetzky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3144-7257","authenticated-orcid":false,"given":"Dhanendra","family":"Tomar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2172-2008","authenticated-orcid":false,"given":"Henry M.","family":"Cohen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shatakshi","family":"Shukla","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manfred","family":"Thomas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salman","family":"Khaledi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4334-6445","authenticated-orcid":false,"given":"Joanne F.","family":"Garbincius","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liam","family":"Kennedy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oniel","family":"Salik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alycia N.","family":"Hildebrand","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3925-2224","authenticated-orcid":false,"given":"John W.","family":"Elrod","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2025092912001201000_2023.10.11.561889v2.1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2005.02.008"},{"key":"2025092912001201000_2023.10.11.561889v2.2","doi-asserted-by":"publisher","DOI":"10.1038\/s41419-017-0215-0"},{"key":"2025092912001201000_2023.10.11.561889v2.3","doi-asserted-by":"publisher","DOI":"10.1038\/emboj.2012.202"},{"key":"2025092912001201000_2023.10.11.561889v2.4","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2019.11.020"},{"key":"2025092912001201000_2023.10.11.561889v2.5","first-page":"184","article-title":"Dysfunctional mitochondrial Ca(2+) handling in mutant SOD1 mouse models of fALS: integration of findings from motor neuron somata and motor terminals","volume":"8","year":"2014","journal-title":"Frontiers in cellular neuroscience"},{"key":"2025092912001201000_2023.10.11.561889v2.6","doi-asserted-by":"publisher","DOI":"10.1038\/nature10234"},{"key":"2025092912001201000_2023.10.11.561889v2.7","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1999.0721030.x"},{"key":"2025092912001201000_2023.10.11.561889v2.8","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000005807"},{"key":"2025092912001201000_2023.10.11.561889v2.9","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-14-05840.2002"},{"key":"2025092912001201000_2023.10.11.561889v2.10","doi-asserted-by":"crossref","first-page":"1345","DOI":"10.3233\/JAD-170543","article-title":"Oxidative Stress, Amyloid-beta Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer\u2019s Disease","volume":"62","year":"2018","journal-title":"Journal of Alzheimer\u2019s disease: JAD"},{"key":"2025092912001201000_2023.10.11.561889v2.11","doi-asserted-by":"crossref","unstructured":"Cai H QJ , Chen S , Yang J , H\u00f6lscher C , Wang Z , Qi J , Wu M . 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