{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:59:04Z","timestamp":1777395544711,"version":"3.51.4"},"reference-count":68,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2018,3,24]],"date-time":"2018-03-24T00:00:00Z","timestamp":1521849600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2018,3,27]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      Low cerebrospinal fluid (CSF) levels of A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      may be the earliest manifestation of Alzheimer\u2019s disease (AD). Knowledge on how CSF A\u03b2 interacts with different brain pathologies early in the disease process is limited. We examined how CSF A\u03b2 markers relate to brain atrophy and white matter lesions (WMLs) in octogenarians with and without dementia to explore the earliest pathogenetic pathways of AD in the oldest old.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To study CSF amyloid biomarkers in relation to brain atrophy and WMLs in 85-year-olds with and without dementia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      53 octogenarians took part in neuropsychiatric examinations and underwent both a lumbar puncture and a brain CT scan. CSF levels of A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      and A\u03b2\n                      <jats:sub>40<\/jats:sub>\n                      were examined in relation to cerebral atrophy and WMLs. Dementia was diagnosed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      In 85-year-olds without dementia, lower levels of both CSF A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      and CSF A\u03b2\n                      <jats:sub>40<\/jats:sub>\n                      were associated with WMLs. CSF A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      also correlated with measures of central atrophy, but not with cortical atrophy. In participants with dementia, lower CSF levels of A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      were related to frontal, temporal, and parietal cortical atrophy but not to WMLs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>\n                      Our findings may suggest that there is an interrelationship between A\u03b2 and subcortical WMLs in older persons without dementia. After onset of dementia, low CSF A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      , probably representing amyloid deposition in plaques, is associated with cortical atrophy. WMLs may be an earlier manifestation of A\u03b2 deposition than cortical degeneration.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-170950","type":"journal-article","created":{"date-parts":[[2018,3,27]],"date-time":"2018-03-27T15:50:57Z","timestamp":1522165857000},"page":"1877-1886","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":16,"title":["Low Cerebrospinal Fluid A\u03b2\n                    <sub>42<\/sub>\n                    and A\u03b2\n                    <sub>40<\/sub>\n                    are Related to White Matter Lesions in Cognitively Normal Elderly"],"prefix":"10.1177","volume":"62","author":[{"given":"Ingmar","family":"Skoog","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Silke","family":"Kern","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"},{"name":"Department of Psychiatry and Neurochemistry, Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"},{"name":"UCL Institute of Neurology, Queen Square, London, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Svante","family":"\u00d6stling","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne","family":"B\u00f6rjesson-Hanson","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xinxin","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Neuropsychiatric Epidemiology Unit, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of 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