{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T02:42:08Z","timestamp":1781664128597,"version":"3.54.5"},"reference-count":74,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2022,11,8]],"date-time":"2022-11-08T00:00:00Z","timestamp":1667865600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2022,11,8]]},"abstract":"<jats:p>Background: Alzheimer\u2019s disease (AD) research has relied on mouse models overexpressing human mutant A \u03b2PP; however, newer generation knock-in models allow for physiological expression of amyloid-\u03b2 protein precursor (A\u03b2PP) containing familial AD mutations where murine A\u03b2PP is edited with a humanized amyloid-\u03b2 (A\u03b2) sequence. The AppNL-F mouse model has shown substantial similarities to AD brains developing late onset cognitive impairment. Objective: In this study, we aimed to characterize mature primary cortical neurons derived from homozygous AppNL-F embryos, especially to identify early mitochondrial alterations in this model. Methods: Primary cultures of AppNL-F neurons kept in culture for 12\u201315 days were used to measure A\u03b2 levels, secretase activity, mitochondrial functions, mitochondrial-ER contacts, synaptic function, and cell death. Results: We detected higher levels of A\u03b242 released from AppNL-F neurons as compared to wild-type neurons. AppNL-F neurons, also displayed an increased A\u03b242\/A\u03b240 ratio, similar to adult AppNL-F mouse brain. Interestingly, we found an upregulation in mitochondrial oxygen consumption with concomitant downregulation in glycolytic reserve. Furthermore, AppNL-F neurons were more susceptible to cell death triggered by mitochondrial electron transport chain inhibition. Juxtaposition between ER and mitochondria was found to be substantially upregulated, which may account for upregulated mitochondrial-derived ATP production. However, anterograde mitochondrial movement was severely impaired in this model along with loss in synaptic vesicle protein and impairment in pre- and post-synaptic function. Conclusion: We show that widespread mitochondrial alterations can be detected in AppNL-F neurons in vitro, where amyloid plaque deposition does not occur, suggesting soluble and oligomeric A\u03b2-species being responsible for these alterations.<\/jats:p>","DOI":"10.3233\/jad-220383","type":"journal-article","created":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T14:19:17Z","timestamp":1663683557000},"page":"565-583","source":"Crossref","is-referenced-by-count":13,"title":["Mitochondrial Alterations in Neurons Derived from the Murine AppNL-F Knock-In Model of Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"90","author":[{"given":"Giacomo","family":"Dentoni","sequence":"first","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luana","family":"Naia","sequence":"additional","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Portal","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nuno Santos","family":"Leal","sequence":"additional","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per","family":"Nilsson","sequence":"additional","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Lindskog","sequence":"additional","affiliation":[{"name":"Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Ankarcrona","sequence":"additional","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-220383_ref1","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1016\/0165-6147(91)90609-V","article-title":"Amyloid deposition as the central event in the aetiology of Alzheimer\u2019s disease","volume":"12","author":"Hardy","year":"1991","journal-title":"Trends Pharmacol Sci"},{"key":"10.3233\/JAD-220383_ref2","doi-asserted-by":"crossref","first-page":"25","DOI":"10.3389\/fnins.2018.00025","article-title":"Reconsideration of amyloid hypothesis and tau hypothesis in Alzheimer\u2019s disease","volume":"12","author":"Kametani","year":"2018","journal-title":"Front Neurosci"},{"key":"10.3233\/JAD-220383_ref3","doi-asserted-by":"crossref","first-page":"595","DOI":"10.15252\/emmm.201606210","article-title":"The amyloid hypothesis of Alzheimer\u2019s disease at 25 years","volume":"8","author":"Selkoe","year":"2016","journal-title":"EMBO Mol Med"},{"key":"10.3233\/JAD-220383_ref4","doi-asserted-by":"crossref","first-page":"a006320","DOI":"10.1101\/cshperspect.a006320","article-title":"Animal models of Alzheimer disease","volume":"2","author":"LaFerla","year":"2012","journal-title":"Cold Spring Harb Perspect Med"},{"key":"10.3233\/JAD-220383_ref5","doi-asserted-by":"crossref","first-page":"9933","DOI":"10.1523\/JNEUROSCI.1907-16.2016","article-title":"Calpain activation in Alzheimer\u2019s model mice is an artifact of APP and presenilin overexpression","volume":"36","author":"Saito","year":"2016","journal-title":"J Neurosci"},{"key":"10.3233\/JAD-220383_ref6","doi-asserted-by":"crossref","first-page":"3118","DOI":"10.1074\/jbc.M117.811315","article-title":"Endoplasmic reticulum stress responses in mouse models of Alzheimer\u2019s disease: Overexpression paradigm versus knockin paradigm","volume":"293","author":"Hashimoto","year":"2018","journal-title":"J Biol Chem"},{"key":"10.3233\/JAD-220383_ref7","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1038\/nn.3697","article-title":"Single App knock-in mouse models of Alzheimer\u2019s disease","volume":"17","author":"Saito","year":"2014","journal-title":"Nat Neurosci"},{"key":"10.3233\/JAD-220383_ref8","doi-asserted-by":"crossref","first-page":"435","DOI":"10.3389\/fncel.2018.00435","article-title":"Contribution of the endosomal-lysosomal and proteasomal systems in amyloid-beta precursor protein derived fragments processing","volume":"12","author":"Evrard","year":"2018","journal-title":"Front Cell Neurosci"},{"key":"10.3233\/JAD-220383_ref9","doi-asserted-by":"crossref","first-page":"re2","DOI":"10.1126\/sageke.2006.10.re2","article-title":"Targeting the role of the endosome in the pathophysiology of Alzheimer\u2019s disease: A strategy for treatment","volume":"2006","author":"Tate","year":"2006","journal-title":"Sci Aging Knowledge Environ"},{"key":"10.3233\/JAD-220383_ref10","doi-asserted-by":"crossref","first-page":"570","DOI":"10.1002\/bies.201400002","article-title":"Dual roles for autophagy: Degradation and secretion of Alzheimer\u2019s disease Abeta peptide","volume":"36","author":"Nilsson","year":"2014","journal-title":"Bioessays"},{"key":"10.3233\/JAD-220383_ref11","doi-asserted-by":"crossref","first-page":"101464","DOI":"10.1016\/j.arr.2021.101464","article-title":"Autophagy in Alzheimer\u2019s disease pathogenesis: Therapeutic potential and future perspectives","volume":"72","author":"Zhang","year":"2021","journal-title":"Ageing Res Rev"},{"key":"10.3233\/JAD-220383_ref12","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1177\/153331750401900205","article-title":"Mitochondrial alterations in Alzheimer\u2019s disease","volume":"19","author":"Baloyannis","year":"2004","journal-title":"Am J Alzheimers Dis Other Demen"},{"key":"10.3233\/JAD-220383_ref13","doi-asserted-by":"crossref","first-page":"19067","DOI":"10.1073\/pnas.0705036104","article-title":"Maternal family history of Alzheimer\u2019s disease predisposes to reduced brain glucose metabolism","volume":"104","author":"Mosconi","year":"2007","journal-title":"Proc Natl Acad Sci U S A"},{"key":"10.3233\/JAD-220383_ref14","doi-asserted-by":"crossref","first-page":"15","DOI":"10.4236\/ami.2014.42003","article-title":"FDG and amyloid PET in cognitively normal individuals at risk for late-onset Alzheimer\u2019s disease","volume":"4","author":"Murray","year":"2014","journal-title":"Adv J Mol Imaging"},{"key":"10.3233\/JAD-220383_ref15","doi-asserted-by":"crossref","first-page":"50310","DOI":"10.1074\/jbc.M405600200","article-title":"Amyloid beta-induced changes in nitric oxide production and mitochondrial activity lead to apoptosis","volume":"279","author":"Keil","year":"2004","journal-title":"J Biol Chem"},{"key":"10.3233\/JAD-220383_ref16","doi-asserted-by":"crossref","first-page":"1574","DOI":"10.1016\/j.neurobiolaging.2007.12.005","article-title":"Mitochondrial dysfunction: An early event in Alzheimer pathology accumulates with age in AD transgenic mice","volume":"30","author":"Hauptmann","year":"2009","journal-title":"Neurobiol Aging"},{"key":"10.3233\/JAD-220383_ref17","doi-asserted-by":"crossref","first-page":"20057","DOI":"10.1073\/pnas.0905529106","article-title":"Amyloid-\u03b2 and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer\u2019s disease mice","volume":"106","author":"Rhein","year":"2009","journal-title":"Proc Natl Acad Sci U S A"},{"key":"10.3233\/JAD-220383_ref18","doi-asserted-by":"crossref","first-page":"91","DOI":"10.1046\/j.0022-3042.2001.00681.x","article-title":"Beta-amyloid inhibits integrated mitochondrial respiration and key enzyme activities","volume":"80","author":"Casley","year":"2002","journal-title":"J Neurochem"},{"key":"10.3233\/JAD-220383_ref19","doi-asserted-by":"crossref","first-page":"607","DOI":"10.1038\/nrm3440","article-title":"Endoplasmic reticulum\u2013mitochondria contacts: Function of the junction","volume":"13","author":"Rowland","year":"2012","journal-title":"Nat Rev Mol Cell Biol"},{"key":"10.3233\/JAD-220383_ref20","doi-asserted-by":"crossref","first-page":"1763","DOI":"10.1126\/science.280.5370.1763","article-title":"Close contacts with the endoplasmic reticulum as determinants of mitochondrial Ca2+ responses","volume":"280","author":"Rizzuto","year":"1998","journal-title":"Science"},{"key":"10.3233\/JAD-220383_ref21","doi-asserted-by":"crossref","first-page":"13807","DOI":"10.1073\/pnas.96.24.13807","article-title":"Regulation of mitochondrial ATP synthesis by calcium: Evidence for a long-term metabolic priming","volume":"96","author":"Jouaville","year":"1999","journal-title":"Proc Natl Acad Sci U S A"},{"key":"10.3233\/JAD-220383_ref22","doi-asserted-by":"crossref","first-page":"270","DOI":"10.1016\/j.cell.2010.06.007","article-title":"Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+transfer to mitochondria","volume":"142","author":"Cardenas","year":"2010","journal-title":"Cell"},{"key":"10.3233\/JAD-220383_ref23","doi-asserted-by":"crossref","first-page":"7248","DOI":"10.1016\/S0021-9258(19)39106-9","article-title":"Phospholipid-synthesis in a membrane-fraction associated with mitochondria","volume":"265","author":"Vance","year":"1990","journal-title":"J Biol Chem"},{"key":"10.3233\/JAD-220383_ref24","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1016\/S0021-9258(18)52406-6","article-title":"Newly made phosphatidylserine and phosphatidylethanolamine are preferentially translocated between rat-liver mitochondria and endoplasmic-reticulum","volume":"266","author":"Vance","year":"1991","journal-title":"J Biol Chem"},{"key":"10.3233\/JAD-220383_ref25","doi-asserted-by":"crossref","first-page":"556","DOI":"10.1038\/emboj.2010.346","article-title":"Fis1 and Bap31 bridge the mitochondria-ER interface to establish a platform for apoptosis induction","volume":"30","author":"Iwasawa","year":"2011","journal-title":"EMBO J"},{"key":"10.3233\/JAD-220383_ref26","doi-asserted-by":"crossref","first-page":"358","DOI":"10.1126\/science.1207385","article-title":"ER tubules mark sites of mitochondrial division","volume":"334","author":"Friedman","year":"2011","journal-title":"Science"},{"key":"10.3233\/JAD-220383_ref27","doi-asserted-by":"crossref","first-page":"389","DOI":"10.1038\/nature11910","article-title":"Autophagosomes form at ER-mitochondria contact sites","volume":"495","author":"Hamasaki","year":"2013","journal-title":"Nature"},{"key":"10.3233\/JAD-220383_ref28","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1038\/nature09663","article-title":"A role for mitochondria in NLRP3 inflammasome activation","volume":"469","author":"Zhou","year":"2011","journal-title":"Nature"},{"key":"10.3233\/JAD-220383_ref29","doi-asserted-by":"crossref","first-page":"7916","DOI":"10.1073\/pnas.1300677110","article-title":"Modulation of the endoplasmic reticulum-mitochondria interface in Alzheimer\u2019s disease and related models","volume":"110","author":"Hedskog","year":"2013","journal-title":"Proc Natl Acad Sci U S A"},{"key":"10.3233\/JAD-220383_ref30","doi-asserted-by":"crossref","first-page":"1810","DOI":"10.2353\/ajpath.2009.090219","article-title":"Presenilins are enriched in endoplasmic reticulum membranes associated with mitochondria","volume":"175","author":"Area-Gomez","year":"2009","journal-title":"Am J Pathol"},{"key":"10.3233\/JAD-220383_ref31","doi-asserted-by":"crossref","first-page":"1549","DOI":"10.3233\/JAD-160953","article-title":"Localization and processing of the amyloid-beta protein precursor in mitochondria-associated membranes","volume":"55","author":"Del Prete","year":"2017","journal-title":"J Alzheimers Dis"},{"key":"10.3233\/JAD-220383_ref32","doi-asserted-by":"crossref","first-page":"2552","DOI":"10.3390\/cells9122552","article-title":"Amyloid \u03b2-peptide increases mitochondria-endoplasmic reticulum contact altering mitochondrial function and autophagosome formation in Alzheimer\u2019s disease-related models","volume":"9","author":"Leal","year":"2020","journal-title":"Cells"},{"key":"10.3233\/JAD-220383_ref33","doi-asserted-by":"crossref","first-page":"369","DOI":"10.3233\/JAD-132543","article-title":"Amyloid-beta peptides are generated in mitochondria-associated endoplasmic reticulum membranes","volume":"43","author":"Schreiner","year":"2015","journal-title":"J Alzheimers Dis"},{"key":"10.3233\/JAD-220383_ref34","doi-asserted-by":"crossref","first-page":"371","DOI":"10.1016\/j.cub.2016.12.038","article-title":"The ER-mitochondria tethering complex VAPB-PTPIP51 regulates autophagy","volume":"27","author":"Gomez-Suaga","year":"2017","journal-title":"Curr Biol"},{"key":"10.3233\/JAD-220383_ref35","doi-asserted-by":"crossref","first-page":"a006270","DOI":"10.1101\/cshperspect.a006270","article-title":"Trafficking and proteolytic processing of APP","volume":"2","author":"Haass","year":"2012","journal-title":"Cold Spring Harb Perspect Med"},{"key":"10.3233\/JAD-220383_ref36","doi-asserted-by":"crossref","first-page":"3885","DOI":"10.1038\/s41467-019-11813-6","article-title":"Impaired mitochondrial calcium efflux contributes to disease progression in models of Alzheimer\u2019s disease","volume":"10","author":"Jadiya","year":"2019","journal-title":"Nat Commun"},{"key":"10.3233\/JAD-220383_ref37","doi-asserted-by":"crossref","first-page":"672","DOI":"10.1038\/360672a0","article-title":"Mutation of the \u03b2-amyloid precursor protein in familial Alzheimer\u2019s disease increases \u03b2-protein production","volume":"360","author":"Citron","year":"1992","journal-title":"Nature"},{"key":"10.3233\/JAD-220383_ref38","doi-asserted-by":"crossref","first-page":"S405","DOI":"10.1016\/S0197-4580(04)81327-7","article-title":"Mitochondrial alterations in Alzheimer\u2019s disease","volume":"25","author":"Baloyannis","year":"2004","journal-title":"Neurobiol Aging"},{"key":"10.3233\/JAD-220383_ref39","doi-asserted-by":"crossref","first-page":"240","DOI":"10.1016\/j.molcel.2016.05.040","article-title":"Redox nanodomains are induced by and control calcium signaling at the ER-mitochondrial interface","volume":"63","author":"Booth","year":"2016","journal-title":"Mol Cell"},{"key":"10.3233\/JAD-220383_ref40","doi-asserted-by":"crossref","first-page":"441","DOI":"10.1016\/j.bbalip.2008.07.004","article-title":"Lipid droplet-organelle interactions; sharing the fats","volume":"1791","author":"Murphy","year":"2009","journal-title":"Biochim Biophys Acta"},{"key":"10.3233\/JAD-220383_ref41","doi-asserted-by":"crossref","first-page":"4106","DOI":"10.1038\/emboj.2012.202","article-title":"Upregulated function of mitochondria-associated ER membranes in Alzheimer disease","volume":"31","author":"Area-Gomez","year":"2012","journal-title":"EMBO J"},{"key":"10.3233\/JAD-220383_ref42","doi-asserted-by":"crossref","first-page":"1686","DOI":"10.1111\/jcmm.12863","article-title":"Mitofusin-2 knockdown increases ER-mitochondria contact and decreases amyloid beta-peptide production","volume":"20","author":"Leal","year":"2016","journal-title":"J Cell Mol Med"},{"key":"10.3233\/JAD-220383_ref43","doi-asserted-by":"crossref","first-page":"2174","DOI":"10.1073\/pnas.1504880112","article-title":"Mitofusin 2 ablation increases endoplasmic reticulum-mitochondria coupling. , E","volume":"112","author":"Filadi","year":"2015","journal-title":"Proc Natl Acad Sci U S A"},{"key":"10.3233\/JAD-220383_ref44","doi-asserted-by":"crossref","first-page":"105020","DOI":"10.1016\/j.nbd.2020.105020","article-title":"Disruption of endoplasmic reticulum-mitochondria tethering proteins in post-mortem Alzheimer\u2019s disease brain","volume":"143","author":"Lau","year":"2020","journal-title":"Neurobiol Dis"},{"key":"10.3233\/JAD-220383_ref45","doi-asserted-by":"crossref","first-page":"789","DOI":"10.1126\/science.1074069","article-title":"Alzheimer\u2019s disease is a synaptic failure","volume":"298","author":"Selkoe","year":"2002","journal-title":"Science"},{"key":"10.3233\/JAD-220383_ref46","doi-asserted-by":"crossref","first-page":"1147","DOI":"10.1016\/S0092-8674(00)81459-2","article-title":"Targeted disruption of mouse conventional kinesin heavy chain, kif5B, results in abnormal perinuclear clustering of mitochondria","volume":"93","author":"Tanaka","year":"1998","journal-title":"Cell"},{"key":"10.3233\/JAD-220383_ref47","doi-asserted-by":"crossref","first-page":"301","DOI":"10.1016\/j.mcn.2008.10.016","article-title":"GTPase dependent recruitment of Grif-1 by Miro1 regulates mitochondrial trafficking in hippocampal neurons","volume":"40","author":"MacAskill","year":"2009","journal-title":"Mol Cell Neurosci"},{"key":"10.3233\/JAD-220383_ref48","doi-asserted-by":"crossref","first-page":"18079","DOI":"10.1074\/jbc.M111.236018","article-title":"Trafficking kinesin protein (TRAK)-mediated transport of mitochondria in axons of hippocampal neurons","volume":"286","author":"Brickley","year":"2011","journal-title":"J Biol Chem"},{"key":"10.3233\/JAD-220383_ref49","doi-asserted-by":"crossref","first-page":"69","DOI":"10.1002\/msj.20159","article-title":"Transgenic mouse models of Alzheimer\u2019s disease","volume":"77","author":"Elder","year":"2010","journal-title":"Mt Sinai J Med"},{"key":"10.3233\/JAD-220383_ref50","doi-asserted-by":"crossref","first-page":"2473","DOI":"10.15252\/embj.201797397","article-title":"APP mouse models for Alzheimer\u2019s disease preclinical studies","volume":"36","author":"Sasaguri","year":"2017","journal-title":"EMBO J"},{"key":"10.3233\/JAD-220383_ref51","doi-asserted-by":"crossref","first-page":"2421","DOI":"10.1038\/s41467-021-22624-z","article-title":"Generation of a humanized A\u03b2 expressing mouse demonstrating aspects of Alzheimer\u2019s disease-like pathology","volume":"12","author":"Baglietto-Vargas","year":"2021","journal-title":"Nat Commun"},{"key":"10.3233\/JAD-220383_ref52","doi-asserted-by":"crossref","first-page":"257","DOI":"10.1007\/s00401-016-1577-6","article-title":"Intraneuronal aggregation of the \u03b2-CTF fragment of APP (C99) induces A\u03b2-independent lysosomal-autophagic pathology","volume":"132","author":"Lauritzen","year":"2016","journal-title":"Acta Neuropathol"},{"key":"10.3233\/JAD-220383_ref53","doi-asserted-by":"crossref","first-page":"1240","DOI":"10.1016\/j.bbadis.2013.10.015","article-title":"Oxidative stress and mitochondrial dysfunction in Alzheimer\u2019s disease","volume":"1842","author":"Wang","year":"2014","journal-title":"Biochim Biophys Acta"},{"key":"10.3233\/JAD-220383_ref54","doi-asserted-by":"crossref","first-page":"2552","DOI":"10.3390\/cells9122552","article-title":"Amyloid \u03b2-peptide increases mitochondria-endoplasmic reticulum contact altering mitochondrial function and autophagosome formation in Alzheimer\u2019s disease-related models","volume":"9","author":"Leal","year":"2020","journal-title":"Cells"},{"key":"10.3233\/JAD-220383_ref55","doi-asserted-by":"crossref","first-page":"510","DOI":"10.1016\/j.jalz.2016.09.003","article-title":"Nuclear but not mitochondrial-encoded oxidative phosphorylation genes are altered in aging, mild cognitive impairment, and Alzheimer\u2019s disease","volume":"13","author":"Mastroeni","year":"2017","journal-title":"Alzheimers Dement"},{"key":"10.3233\/JAD-220383_ref56","doi-asserted-by":"crossref","first-page":"1417","DOI":"10.1038\/cdd.2016.52","article-title":"The coming of age of the mitochondria-ER contact: A matter of thickness","volume":"23","author":"Giacomello","year":"2016","journal-title":"Cell Death Diff"},{"key":"10.3233\/JAD-220383_ref57","first-page":"bio047530","article-title":"Forcing contacts between mitochondria and the endoplasmic reticulum extends lifespan in a Drosophila model of Alzheimer\u2019s disease","volume":"9","author":"Garrido-Maraver","year":"2020","journal-title":"Biol Open"},{"key":"10.3233\/JAD-220383_ref58","doi-asserted-by":"crossref","first-page":"915","DOI":"10.1083\/jcb.200604016","article-title":"Structural and functional features and significance of the physical linkage between ER and mitochondria","volume":"174","author":"Csordas","year":"2006","journal-title":"J Cell Biol"},{"key":"10.3233\/JAD-220383_ref59","doi-asserted-by":"crossref","first-page":"20796","DOI":"10.1074\/jbc.M109.025353","article-title":"Calcium elevation in mitochondria is the main Ca2+ requirement formitochondrial permeability transition pore (mPTP) opening","volume":"284","author":"Baumgartner","year":"2009","journal-title":"JBiol Chem"},{"key":"10.3233\/JAD-220383_ref60","doi-asserted-by":"crossref","first-page":"1133","DOI":"10.1097\/00004647-200110000-00001","article-title":"An energy budget for signaling in the grey matter of the brain","volume":"21","author":"Attwell","year":"2001","journal-title":"J Cereb Blood Flow Metab"},{"key":"10.3233\/JAD-220383_ref61","doi-asserted-by":"crossref","first-page":"137","DOI":"10.1016\/j.cell.2007.11.024","article-title":"Docking of axonal mitochondria by syntaphilin controls their mobility and affects short-term facilitation","volume":"132","author":"Kang","year":"2008","journal-title":"Cell"},{"key":"10.3233\/JAD-220383_ref62","doi-asserted-by":"crossref","first-page":"4515","DOI":"10.1093\/hmg\/ddr381","article-title":"Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer\u2019s disease","volume":"20","author":"Calkins","year":"2011","journal-title":"Hum Mol Genet"},{"key":"10.3233\/JAD-220383_ref63","doi-asserted-by":"crossref","first-page":"2495","DOI":"10.1093\/hmg\/ddr139","article-title":"Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer\u2019s disease: Implications for neuronal damage","volume":"20","author":"Manczak","year":"2011","journal-title":"Hum Mol Genet"},{"key":"10.3233\/JAD-220383_ref64","doi-asserted-by":"crossref","first-page":"814","DOI":"10.1016\/j.bbadis.2015.12.018","article-title":"Multiple faces of dynamin-related protein 1 and its role in Alzheimer\u2019s disease pathogenesis","volume":"1862","author":"Kandimalla","year":"2016","journal-title":"Biochim Biophys Acta"},{"key":"10.3233\/JAD-220383_ref65","doi-asserted-by":"crossref","first-page":"9090","DOI":"10.1523\/JNEUROSCI.1357-09.2009","article-title":"Impaired balance of mitochondrial fission and fusion in Alzheimer\u2019s disease","volume":"29","author":"Wang","year":"2009","journal-title":"J Neurosci"},{"key":"10.3233\/JAD-220383_ref66","doi-asserted-by":"crossref","first-page":"13275","DOI":"10.1523\/JNEUROSCI.1034-15.2015","article-title":"Neuronal store-operated calcium entry and mushroom spine loss in amyloid precursor protein knock-in mouse model of Alzheimer\u2019s disease","volume":"35","author":"Zhang","year":"2015","journal-title":"J Neurosci"},{"key":"10.3233\/JAD-220383_ref67","doi-asserted-by":"crossref","first-page":"157","DOI":"10.1038\/s41422-021-00582-x","article-title":"An App knock-in rat model for Alzheimer\u2019s disease exhibiting A\u03b2 and tau pathologies, neuronal death and cognitive impairments","volume":"32","author":"Pang","year":"2022","journal-title":"Cell Res"},{"key":"10.3233\/JAD-220383_ref68","first-page":"5557","article-title":"Impaired spike-gamma coupling of area CA3fast-spiking interneurons as the earliest functional impairment inthe AppNL-G-F mouse model of Alzheimer\u2019s disease","volume":"26","author":"Arroyo-Garc\u00eda","year":"2021","journal-title":"MolPsychiatry"},{"key":"10.3233\/JAD-220383_ref69","doi-asserted-by":"crossref","first-page":"141","DOI":"10.1016\/j.cels.2020.11.007","article-title":"Pulse-chase proteomics of the App knockin mouse models of Alzheimer\u2019s disease reveals that synaptic dysfunction originates in presynaptic terminals","volume":"12","author":"Hark","year":"2021","journal-title":"Cell Syst"},{"key":"10.3233\/JAD-220383_ref71","doi-asserted-by":"crossref","first-page":"4399","DOI":"10.1038\/s41467-019-12382-4","article-title":"Miro clusters regulate ER-mitochondria contact sites and link cristae organization to the mitochondrial transport machinery","volume":"10","author":"Modi","year":"2019","journal-title":"Nat Commun"},{"key":"10.3233\/JAD-220383_ref72","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1083\/jcb.200406038","article-title":"Control of mitochondrial motility and distribution by the calcium signal: A homeostatic circuit","volume":"167","author":"Yi","year":"2004","journal-title":"J Cell Biol"},{"key":"10.3233\/JAD-220383_ref73","doi-asserted-by":"crossref","first-page":"98","DOI":"10.1016\/j.brainres.2015.10.005","article-title":"Induced pluripotent stem cells as a discovery tool for Alzheimer\u2019s disease","volume":"1656","author":"Sullivan","year":"2017","journal-title":"Brain Res"},{"key":"10.3233\/JAD-220383_ref74","doi-asserted-by":"crossref","first-page":"84","DOI":"10.1186\/s12864-015-1262-5","article-title":"Induced pluripotent stem cell-derived neuronal cells from a sporadic Alzheimer\u2019s disease donor as a model for investigating AD-associated gene regulatory networks","volume":"16","author":"Hossini","year":"2015","journal-title":"BMC Genomics"},{"key":"10.3233\/JAD-220383_ref75","doi-asserted-by":"crossref","first-page":"401","DOI":"10.1038\/s41593-018-0332-9","article-title":"Mitophagy inhibits amyloid-\u03b2 and tau pathology and reverses cognitive deficits in models of Alzheimer\u2019s disease","volume":"22","author":"Fang","year":"2019","journal-title":"Nat Neurosci"}],"container-title":["Journal of Alzheimer's Disease"],"original-title":[],"link":[{"URL":"https:\/\/content.iospress.com\/download?id=10.3233\/JAD-220383","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T10:07:35Z","timestamp":1777370855000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/full\/10.3233\/JAD-220383"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022,11,8]]},"references-count":74,"journal-issue":{"issue":"2"},"URL":"https:\/\/doi.org\/10.3233\/jad-220383","relation":{},"ISSN":["1387-2877","1875-8908"],"issn-type":[{"value":"1387-2877","type":"print"},{"value":"1875-8908","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022,11,8]]}}}