{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T17:23:18Z","timestamp":1793035398662,"version":"4.5.0"},"reference-count":92,"publisher":"Scientific Scholar","issue":"2","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,8]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Late-onset Alzheimer's disease (LOAD) or sporadic AD is the most common form of AD. The precise pathogenetic changes that trigger the development of AD remain largely unknown. Large-scale genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms in multiple genes which are associated with AD; most notably, these are <jats:italic toggle=\"yes\">ABCA7<\/jats:italic>, bridging integrator 1(<jats:italic toggle=\"yes\">B1N1<\/jats:italic>), triggering receptor expressed on myeloid cells 2 (<jats:italic toggle=\"yes\">TREM2<\/jats:italic>), <jats:italic toggle=\"yes\">CD33<\/jats:italic>, clusterin (<jats:italic toggle=\"yes\">CLU<\/jats:italic>), complement receptor 1 (<jats:italic toggle=\"yes\">CRI<\/jats:italic>), ephrin type-A receptor 1 (EPHA1), membrane-spanning 4-domains, subfamily A (<jats:italic toggle=\"yes\">MS4A<\/jats:italic>) and phosphatidylinositol binding clathrin assembly protein (<jats:italic toggle=\"yes\">PICALM<\/jats:italic>) genes. The proteins coded by the candidate genes participate in a variety of cellular processes such as oxidative balance, protein metabolism, cholesterol metabolism and synaptic function. This review summarizes the major gene loci affecting LOAD identified by large GWASs. Tentative mechanisms have also been elaborated in various studies by which the proteins coded by these genes may exert a role in AD pathogenesis have also been elaborated. The review suggests that these may together affect LOAD pathogenesis in a complementary fashion.<\/jats:p>\n          <\/jats:sec>","DOI":"10.4103\/ijmr.ijmr_473_17","type":"journal-article","created":{"date-parts":[[2018,10,19]],"date-time":"2018-10-19T04:55:27Z","timestamp":1539924927000},"page":"135-144","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":33,"title":["New genetic players in late-onset Alzheimer's disease"],"prefix":"10.25259","volume":"148","author":[{"given":"Anamika","family":"Misra","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sankha Shubhra","family":"Chakrabarti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Indrajeet 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