{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T05:17:27Z","timestamp":1791955047908,"version":"4.3.4"},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,2,12]],"date-time":"2017-02-12T00:00:00Z","timestamp":1486857600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      Both amyloid deposition and neuroinflammation appear in the early course of Alzheimer's disease (\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      ). However, the progression of neuroinflammation and its relationship with amyloid deposition and behavioral changes have not been fully elucidated. A better understanding the role of neuroinflammation in\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      might extend our current knowledge to therapeutic intervention possibilities.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This study systematically characterized changes in behavioral abnormalities in\n                      <jats:styled-content style=\"fixed-case\">APP<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">PS<\/jats:styled-content>\n                      1 transgenic mice. Brain pathology measures were performed in post\u2010mortem brain tissues of mice from 2 to 22\u00a0months.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">APP<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">PS<\/jats:styled-content>\n                      1 mice exhibited significant memory deficits from 5\u00a0months old, which were aggravated at the later stage of life. However, the degree of memory impairments reached a plateau at 12\u00a0months. An early appearance of amyloid plaques was at 3\u00a0months with a linear increase throughout the disease course.\n                      <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                      11b\u2010positive microglia and glial fibrillary acidic protein\u2010(\n                      <jats:styled-content style=\"fixed-case\">GFAP<\/jats:styled-content>\n                      ) positive astrocytes were first detected at 3\u00a0months with a close association with amyloid plaques. Yet, the rate of changes in glial activation slowed down from 12\u00a0months despite the steady increase in A\u03b2.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These findings provided evidence that neuroinflammation might be involved in the development and progression of cognitive deficits in\n                      <jats:styled-content style=\"fixed-case\">APP<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">PS<\/jats:styled-content>\n                      1 mice, suggesting novel intervention and prevention strategies for\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/cns.12677","type":"journal-article","created":{"date-parts":[[2017,2,12]],"date-time":"2017-02-12T23:16:42Z","timestamp":1486941402000},"page":"310-320","source":"Crossref","is-referenced-by-count":93,"title":["The role of neuroinflammation and amyloid in cognitive impairment in an\n                    <scp>APP<\/scp>\n                    \/\n                    <scp>PS<\/scp>\n                    1 transgenic mouse model of Alzheimer's disease"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2238-4960","authenticated-orcid":false,"given":"Shenghua","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Therapeutics Max Rady College of Medicine Rady Faculty of Health Sciences University of Manitoba  Winnipeg MB Canada"},{"name":"Kleysen Institute for Advanced Medicine Health Sciences Centre  Winnipeg MB 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