{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T01:09:51Z","timestamp":1789952991218,"version":"4.0.1"},"reference-count":39,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2015,8,11]],"date-time":"2015-08-11T00:00:00Z","timestamp":1439251200000},"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":[[2015,8,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Caffeine may be protective against Alzheimer\u2019s disease (AD) by modulating amyloid-\u03b2 (A\u03b2) metabolic pathways. The present work aimed to study a possible association of caffeine consumption with the cerebrospinal fluid (CSF) biomarkers, particularly A\u03b2. The study included 88 patients with AD or mild cognitive impairment. The consumption of caffeine and theobromine was evaluated using a validated food questionnaire. Quantification of caffeine and main active metabolites was performed with liquid chromatography coupled to tandem mass spectrometry. The levels of A\u03b2\n                    <jats:sub>1\u00a0-\u00a042<\/jats:sub>\n                    , total tau, and phosphorylated tau in the CSF were determined using sandwich ELISA methods and other A\u03b2 species, A\u03b2\n                    <jats:sub>X\u00a0-\u00a038<\/jats:sub>\n                    , A\u03b2\n                    <jats:sub>X\u00a0-\u00a040<\/jats:sub>\n                    , and A\u03b2\n                    <jats:sub>X\u00a0-\u00a042<\/jats:sub>\n                    , with the MSD A\u03b2 Triplex assay. The concentration of caffeine was 0.79\u00b11.15\n                    <jats:italic>\u03bc<\/jats:italic>\n                    g\/mL in the CSF and 1.20\u00b11.88\n                    <jats:italic>\u03bc<\/jats:italic>\n                    g\/mL in the plasma. No correlation was found between caffeine consumption and A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    in the CSF. However, a significant positive correlation was found between the concentrations of theobromine, both in the CSF and in the plasma, with A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    in the CSF. Theobromine in the CSF was positively correlated with the levels of other xanthines in the CSF, but not in the plasma, suggesting that it may be formed by central metabolic pathways. In conclusion, caffeine consumption does not modify the levels of CSF biomarkers, and does not require to be controlled for when measuring CSF biomarkers in a clinical setting. Since theobromine is associated with a favorable A\u03b2 profile in the CSF, the possibility that it might have a protective role in AD should be further investigated.\n                  <\/jats:p>","DOI":"10.3233\/jad-150374","type":"journal-article","created":{"date-parts":[[2015,8,13]],"date-time":"2015-08-13T09:29:49Z","timestamp":1439458189000},"page":"1069-1078","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":32,"title":["Does Caffeine Consumption Modify Cerebrospinal Fluid Amyloid-\u03b2 Levels in\u00a0Patients with Alzheimer\u2019s Disease?"],"prefix":"10.1177","volume":"47","author":[{"given":"Maria","family":"Travassos","sequence":"first","affiliation":[{"name":"Institute of Molecular Medicine and Faculty of Medicine, University of Lisbon, Lisbon, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabel","family":"Santana","sequence":"additional","affiliation":[{"name":"Department 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Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00f6rsev G.","family":"Yener","sequence":"additional","affiliation":[{"name":"Dokuz Eylul University, Department of Neurology and Brain Dynamics Center, Izmir, Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anja","family":"Simonsen","sequence":"additional","affiliation":[{"name":"Danish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steen G.","family":"Hasselbalch","sequence":"additional","affiliation":[{"name":"Danish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabeth","family":"Kapaki","sequence":"additional","affiliation":[{"name":"Department of Neurology, Faculty of Medicine, National and Kapodistrian University of Athens, Athens, 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