{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T16:47:59Z","timestamp":1787071679743,"version":"build-2736575974"},"reference-count":92,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>\n                    The overexpression of the amyloid precursor protein (\n                    <jats:italic toggle=\"yes\">APP<\/jats:italic>\n                    ) gene, encoded on chromosome 21, has been associated in Down syndrome (DS) with the development of early-onset Alzheimer's disease (EOAD). The increase in\n                    <jats:italic toggle=\"yes\">APP<\/jats:italic>\n                    levels leads to an overproduction of amyloid-\u03b2 (A\u03b2) peptide that accumulates in the brain. In response to this deposition, microglial cells are active and generate cascade events that include release cytokines and chemokine. The prolonged activation microglial cells induce neuronal loss, production of reactive oxygen species, neuron death, neuroinflammation, and consequently the development of Alzheimer's disease (AD). The intrinsically deficient immune systems in people with DS result in abnormalities in cytokine levels, which possibly contribute to the development of neurodegenerative disorders such as AD. Knowledge about the biomarkers involved in the process of neurodegeneration and neuroinflamation is important for understanding the mechanisms involved in the incidence and the precocity of AD in individuals with DS.\n                  <\/jats:p>","DOI":"10.4103\/0028-3886.310062","type":"journal-article","created":{"date-parts":[[2021,4,26]],"date-time":"2021-04-26T01:22:00Z","timestamp":1619400120000},"page":"32-41","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":8,"title":["Alzheimer's Disease in the Down Syndrome: An Overview of Genetics and Molecular Aspects"],"prefix":"10.4103","volume":"69","author":[{"given":"Fabiana de C","family":"Gomes","sequence":"first","affiliation":[{"name":"Genetics and Molecular Biology Research Unit (UPGEM), Department of Molecular Biology, S\u00e3o Jos\u00e9 do Rio Preto Medical School (FAMERP), S\u00e3o Jos\u00e9 do Rio Preto \u2013 SP, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marlon F","family":"Mattos","sequence":"additional","affiliation":[{"name":"Genetics and Molecular Biology Research Unit (UPGEM), Department of Molecular Biology, S\u00e3o Jos\u00e9 do Rio Preto Medical School (FAMERP), S\u00e3o Jos\u00e9 do Rio Preto \u2013 SP, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eny M","family":"Goloni-Bertollo","sequence":"additional","affiliation":[{"name":"Genetics and Molecular Biology Research Unit (UPGEM), Department of Molecular Biology, S\u00e3o Jos\u00e9 do Rio Preto Medical School (FAMERP), S\u00e3o Jos\u00e9 do Rio Preto \u2013 SP, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c9rika C","family":"Pavarino","sequence":"additional","affiliation":[{"name":"Genetics and Molecular Biology Research Unit (UPGEM), Department of Molecular Biology, S\u00e3o Jos\u00e9 do Rio Preto Medical School (FAMERP), S\u00e3o Jos\u00e9 do Rio 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