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Concentrations of leptin, soluble leptin receptor (sOB\u2010R), and their ratio (free leptin index [FLI]), indicating leptin bioavailability, were measured using enzyme\u2010linked immunosorbent assays. Cognitive and MRI measures were derived using standardized protocols.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      Higher sOB\u2010R was associated with lower fractional anisotropy (FA,\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a0\u22120.114\u00a0\u00b1\u00a00.02,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001), and higher free water (FW,\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a00.091\u00a0\u00b1\u00a00.022,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001) and peak\u2010width skeletonized mean diffusivity (PSMD,\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a00.078\u00a0\u00b1\u00a00.021,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001). Correspondingly, higher FLI was associated with higher FA (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a00.115\u00a0\u00b1\u00a00.027,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&lt;\u00a00.001) and lower FW (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a0\u20100.096\u00a0\u00b1\u00a00.029,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a00.001) and PSMD (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u00a0=\u00a0\u20100.085\u00a0\u00b1\u00a00.028,\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0=\u00a00.002).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>Higher leptin bioavailability was associated with better white matter (WM) integrity in healthy middle\u2010aged adults, supporting the putative neuroprotective role of leptin in late\u2010life dementia risk.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Higher leptin bioavailability was related to better preservation of white matter microstructure.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Higher leptin bioavailability during midlife might confer protection against dementia.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Potential benefits might be even stronger for individuals with visceral obesity.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>DTI measures might be sensitive surrogate markers of subclinical neuropathology.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.13879","type":"journal-article","created":{"date-parts":[[2024,8,12]],"date-time":"2024-08-12T07:00:15Z","timestamp":1723446015000},"page":"5849-5860","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Leptin bioavailability and markers of brain atrophy and vascular injury in the middle age"],"prefix":"10.1002","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6578-393X","authenticated-orcid":false,"given":"Sokratis","family":"Charisis","sequence":"first","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meghan I.","family":"Short","sequence":"additional","affiliation":[{"name":"Institute for Clinical Research and Health Policy Studies Tufts Medical Center  Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca","family":"Bernal","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiffany F.","family":"Kautz","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hector A.","family":"Trevi\u00f1o","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Mathews","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angel Gabriel Velarde","family":"Dedi\u00f3s","sequence":"additional","affiliation":[{"name":"Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases UT Health San Antonio  San Antonio Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jazmyn A. 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