{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T14:39:36Z","timestamp":1781102376533,"version":"3.54.1"},"reference-count":28,"publisher":"National Academy of Sciences","issue":"24","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1996,11,26]]},"abstract":"<jats:p>\n                    Presenilin-1 (\n                    <jats:italic>PS-1<\/jats:italic>\n                    ) gene mutations are responsible\n for the majority of the early onset familial forms of Alzheimer disease\n (AD). Neither PS-1\u2019s anatomic distribution in brain nor expression in\n AD have been reported. Using\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization in\n the rat forebrain, we show that PS-1 mRNA expression is primarily in\n cortical and hippocampal neurons, with less expression in subcortical\n structures, in a regional pattern similar to APP695. Excitotoxic\n lesions lead to loss of PS-1 signal. A neuronal pattern of expression\n of PS-1 mRNA was also observed in the human hippocampal formation. AD\n and control levels did not differ. PS-1 is expressed in brain areas\n vulnerable to AD changes more so than in areas spared in AD; however,\n PS-1 expression is not sufficient to mark vulnerable regions.\n Collectively, these data suggest that the neuropathogenic process\n consequent to PS-1 mutations begins in neuronal cell populations.\n                  <\/jats:p>","DOI":"10.1073\/pnas.93.24.14020","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:34:16Z","timestamp":1027679656000},"page":"14020-14024","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":37,"title":["<i>In situ<\/i>\n                    hybridization analysis of presenilin 1 mRNA in Alzheimer disease and in lesioned rat\u2009brain"],"prefix":"10.1073","volume":"93","author":[{"given":"Keith","family":"Page","sequence":"first","affiliation":[{"name":"Neurology Research and Laboratory of Genetics and Aging,\r Massachusetts General Hospital, Harvard Medical School, Fruit Street,\r Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Hollister","sequence":"additional","affiliation":[{"name":"Neurology Research and Laboratory of Genetics and Aging,\r Massachusetts General Hospital, Harvard Medical School, Fruit Street,\r Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolph E.","family":"Tanzi","sequence":"additional","affiliation":[{"name":"Neurology Research and Laboratory of Genetics and Aging,\r Massachusetts General Hospital, Harvard Medical School, Fruit Street,\r Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bradley T.","family":"Hyman","sequence":"additional","affiliation":[{"name":"Neurology Research and Laboratory of Genetics and Aging,\r Massachusetts General Hospital, Harvard Medical School, Fruit Street,\r Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1996,11,26]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.90.5.1977"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/349704a0"},{"key":"e_1_3_2_3_2","first-page":"273","volume":"51","author":"Tanzi R E","year":"1992","unstructured":"R E Tanzi, G Vaula, D M Romano, M Mortilla, T L Huang, et al. 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