{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:44:01Z","timestamp":1786977841665,"version":"build-2736575974"},"reference-count":74,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2019,6,3]],"date-time":"2019-06-03T00:00:00Z","timestamp":1559520000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100010573","name":"Stichting Dioraphte","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100010573","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Human Brain Mapping"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Myelin determines the conduction of neuronal signals along axonal connections in networks of the brain. Loss of myelin integrity in neuronal circuits might result in cognitive decline in Alzheimer's disease (AD). Recently, the ratio of T1\u2010weighted by T2\u2010weighted MRI has been used as a proxy for myelin content in gray matter of the cortex. With this approach, we investigated whether AD dementia patients show lower cortical myelin content (i.e., a lower T1\u2010w\/T2\u2010w ratio value). We selected structural T1\u2010w and T2\u2010w MR images of 293 AD patients and 172 participants with normal cognition (NC). T1\u2010w\/T2\u2010w ratios were computed for the whole brain and within 90 automated anatomical labeling atlas regions using SPM12, compared between groups and correlated with the neuronal injury marker tau in cerebrospinal fluid (CSF) and Mini Mental State Examination (MMSE). In contrast to our hypothesis, AD patients showed higher whole brain T1\u2010w\/T2\u2010w ratios than NC, and regionally in 31 anatomical areas (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u2009.0005;\n                    <jats:italic>d<\/jats:italic>\n                    = 0.21 to 0.48), predominantly in the inferior parietal lobule, angular gyrus, anterior cingulate, and precuneus. Regional higher T1\u2010w\/T2\u2010w values were associated with higher CSF tau concentrations (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u2009.0005;\n                    <jats:italic>r<\/jats:italic>\n                    = .16 to .22) and worse MMSE scores (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u2009.0005;\n                    <jats:italic>r<\/jats:italic>\n                    = \u2212.16 to \u2212.21). These higher T1\u2010w\/T2\u2010w values in AD seem to contradict previous pathological findings of demyelination and disconnectivity in AD. Future research should further investigate the biological processes reflected by increases in T1\u2010w\/T2\u2010w values.\n                  <\/jats:p>","DOI":"10.1002\/hbm.24638","type":"journal-article","created":{"date-parts":[[2019,6,3]],"date-time":"2019-06-03T08:55:21Z","timestamp":1559552121000},"page":"3900-3909","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Gray matter T1\u2010w\/T2\u2010w ratios are higher in Alzheimer's disease"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6708-5374","authenticated-orcid":false,"given":"Wiesje","family":"Pelkmans","sequence":"first","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen","family":"Dicks","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederik","family":"Barkhof","sequence":"additional","affiliation":[{"name":"Department of Radiology &amp; Nuclear Medicine Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"},{"name":"Institutes of Neurology and Healthcare Engineering, UCL  London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hugo","family":"Vrenken","sequence":"additional","affiliation":[{"name":"Department of Radiology &amp; Nuclear Medicine Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip","family":"Scheltens","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wiesje M.","family":"van der Flier","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"},{"name":"Department of Epidemiology &amp; Biostatistics Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Betty M.","family":"Tijms","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC  Amsterdam The 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