{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T08:20:34Z","timestamp":1787559634429,"version":"build-2736575974"},"reference-count":71,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2016,10,11]],"date-time":"2016-10-11T00:00:00Z","timestamp":1476144000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2016,11,19]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Deficits in mitochondrial function and oxidative stress play\n          pivotal roles in Down syndrome (DS) and Alzheimer\u2019s disease (AD) and these alterations in\n          mitochondria occur systemically in both conditions.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Objective:<\/jats:bold>\n                    We hypothesized that peripheral cells of elder subjects with DS\n          exhibit disease-specific and dementia-specific metabolic features. To test this, we\n          performed a comprehensive analysis of energy metabolism in lymphoblastic-cell-lines (LCLs)\n          derived from subjects belonging to four groups: DS-with-dementia (DSAD),\n          DS-without-dementia (DS), sporadic AD, and age-matched controls.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    LCLs were studied under regular or minimal feeding regimes with\n          galactose or glucose as primary carbohydrate sources. We assessed metabolism under\n          glycolysis or oxidative phosphorylation by quantifying cell viability, oxidative stress,\n          ATP levels, mitochondrial membrane potential (MMP), mitochondrial calcium uptake, and\n          autophagy.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    DS and DSAD LCLs showed slower growth rates under minimal feeding.\n          DS LCLs mainly dependent on mitochondrial respiration exhibited significantly slower\n          growth and higher levels of oxidative stress compared to other groups. While ATP levels\n          (under mitochondrial inhibitors) and mitochondrial calcium uptake were significantly\n          reduced in DSAD and AD cells, MMP was decreased in DS, DSAD, and AD LCLs. Finally, DS LCLs\n          showed markedly reduced levels of the autophagy marker LC3-II, underscoring the close\n          association between metabolic dysfunction and impaired autophagy in DS.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    There are significant mitochondrial functional changes in LCLs\n          derived from DS, DSAD, and AD patients. Several parameters analyzed were consistently\n          different between DS, DSAD, and AD lines suggesting that metabolic indicators between LCL\n          groups may be utilized as biomarkers of disease progression and\/or treatment outcomes.\n                  <\/jats:p>","DOI":"10.3233\/jad-160278","type":"journal-article","created":{"date-parts":[[2016,10,11]],"date-time":"2016-10-11T12:07:11Z","timestamp":1476187631000},"page":"737-748","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":19,"title":["Metabolic and Growth Rate Alterations in Lymphoblastic Cell Lines          Discriminate Between Down Syndrome and Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"55","author":[{"given":"Pinar","family":"Coskun","sequence":"first","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo","family":"Helguera","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]},{"name":"Instituto de Investigaci\u00f3n M\u00e9dica Mercedes y Martin Ferreyra","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zahra","family":"Nemati","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan C.","family":"Bohannan","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean","family":"Thomas","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Schriner E.","family":"Samuel","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jocelyn","family":"Argueta","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Doran","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas C.","family":"Wallace","sequence":"additional","affiliation":[{"name":"University of Pennsylvania","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ira T.","family":"Lott","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Busciglio","sequence":"additional","affiliation":[{"name":"University of California","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,10,11]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1989.00520440031017"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1006\/nbdi.1996.0003"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2004.08.005"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2006.06.023"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.autrev.2012.10.013"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1192\/bjp.162.6.811"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0891-5849(98)00137-3"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-7091-6721-2_6"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pnpbp.2008.10.006"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00604-9"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1042\/BJ20101908"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cmet.2012.12.005"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2011.08.008"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1097\/00019052-200404000-00003"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004010050997"},{"key":"e_1_3_3_17_2","first-page":"223","article-title":"Protein levels of human peroxiredoxin subtypes in\n            brains of patients with Alzheimer\u2019s disease and Down syndrome","author":"Kim SH","year":"2001","unstructured":"KimSH, FountoulakisM, CairnsN, LubecG (2001) Protein levels of human peroxiredoxin subtypes in brains of patients with Alzheimer\u2019s disease and Down syndrome. 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