{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T16:38:36Z","timestamp":1777394316473,"version":"3.51.4"},"reference-count":48,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2015,10,27]],"date-time":"2015-10-27T00:00:00Z","timestamp":1445904000000},"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":[[2015,10,27]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Idiopathic normal pressure hydrocephalus (iNPH) is a dementing condition in which Alzheimer\u2019s disease (AD)-related amyloid-\u03b2 (A\u03b2) plaques are frequently observed in the neocortex. iNPH patients with prominent A\u03b2 pathology show AD-related alterations in amyloid-\u03b2 protein precursor (A\u03b2PP) processing resulting from increased\n                    <jats:italic>\u03b3<\/jats:italic>\n                    -secretase activity.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Objectives:<\/jats:bold>\n                    Our goal was to assess potential alterations in the global gene expression profile in the brain of iNPH patients as compared to non-demented controls and to evaluate the levels of the identified targets in the cerebrospinal fluid (CSF) of iNPH patients.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    The genome-wide expression profile of \u223c35,000 probes was assessed in the RNA samples obtained from 22 iNPH patients and eight non-demented control subjects using a microarray chip. The soluble levels of sA\u03b2PP\n                    <jats:italic>\u03b1<\/jats:italic>\n                    , sA\u03b2PP\u03b2, and transthyretin (TTR) were measured from the CSF of 102 iNPH patients using ELISA.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    After correcting the results for multiple testing, significant differences in the expression of\n                    <jats:italic>TTR<\/jats:italic>\n                    and\n                    <jats:italic>A<\/jats:italic>\n                    \u03b2\n                    <jats:italic>PP<\/jats:italic>\n                    were observed between iNPH and control subjects. The mRNA levels of\n                    <jats:italic>TTR<\/jats:italic>\n                    were on average 17-fold lower in iNPH samples compared to control samples. Conversely, the expression level of\n                    <jats:italic>A<\/jats:italic>\n                    \u03b2\n                    <jats:italic>PP<\/jats:italic>\n                    was on average three times higher in iNPH samples as compared to control samples. Interestingly, the expression of\n                    <jats:italic>\u03b1<\/jats:italic>\n                    -secretase (\n                    <jats:italic>ADAM10<\/jats:italic>\n                    ) was also increased in iNPH patients. In the lumbar CSF samples, soluble TTR levels showed a significant positive correlation with sA\u03b2PP\n                    <jats:italic>\u03b1<\/jats:italic>\n                    and sA\u03b2PP\u03b2, but TTR levels did not predict the brain pathology or the shunt response.\n                    <jats:bold>Conclusions:<\/jats:bold>\n                    These findings suggest differences in the expression profile of key factors involved in AD-related cellular events in the brain of iNPH patients.\n                  <\/jats:p>","DOI":"10.3233\/jad-150268","type":"journal-article","created":{"date-parts":[[2015,10,27]],"date-time":"2015-10-27T16:54:36Z","timestamp":1445964876000},"page":"959-968","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":19,"title":["The Expression of Transthyretin and Amyloid-\u03b2 Protein Precursor is Altered in the Brain of Idiopathic Normal Pressure Hydrocephalus Patients"],"prefix":"10.1177","volume":"48","author":[{"given":"Tiina","family":"Laiter\u00e4","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurology, University of Eastern Finland and Department of Neurology, Kuopio University Hospital, Kuopio, Finland"},{"name":"Institute of Clinical Medicine \u2013 Neurosurgery, University of Eastern Finland and Neurosurgery of NeuroCenter, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mitja I.","family":"Kurki","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurosurgery, University of Eastern Finland and Neurosurgery of NeuroCenter, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juha-Pekka","family":"Pursiheimo","sequence":"additional","affiliation":[{"name":"Institute of Biomedicine, University of Turku, Turku, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Clinical Neurochemistry Laboratory, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seppo","family":"Helisalmi","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurology, University of Eastern Finland and Department of Neurology, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tuomas","family":"Rauramaa","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine - Pathology, University of Eastern Finland and Department of Pathology, Kuopio University Hospital, Kuopio, Finland"},{"name":"Department of Pathology, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Irina","family":"Alafuzoff","sequence":"additional","affiliation":[{"name":"Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne M.","family":"Remes","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurology, University of Eastern Finland and Department of Neurology, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hilkka","family":"Soininen","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurology, University of Eastern Finland and Department of Neurology, Kuopio University Hospital, Kuopio, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annakaisa","family":"Haapasalo","sequence":"additional","affiliation":[{"name":"Institute of Clinical Medicine \u2013 Neurology, University of Eastern Finland and Department of Neurology, Kuopio University Hospital, Kuopio, Finland"},{"name":"Department of Neurobiology, A.I. 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