{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:46:54Z","timestamp":1790340414569,"version":"4.1.0"},"reference-count":322,"publisher":"Walter de Gruyter GmbH","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,12,20]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In this review, we discuss the genetic etiologies of Alzheimer\u2019s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein (<jats:italic>APP<\/jats:italic>) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1\/2,<jats:italic>PSEN1\/2<\/jats:italic>and<jats:italic>APP<\/jats:italic>) and late-onset (apolipoprotein E,<jats:italic>ApoE<\/jats:italic>) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.<\/jats:p>","DOI":"10.1515\/revneuro-2017-0036","type":"journal-article","created":{"date-parts":[[2017,9,26]],"date-time":"2017-09-26T10:01:58Z","timestamp":1506420118000},"page":"21-38","source":"Crossref","is-referenced-by-count":27,"title":["Genetic underpinnings in Alzheimer\u2019s disease \u2013 a review"],"prefix":"10.1515","volume":"29","author":[{"given":"Ahmed A.","family":"Moustafa","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mubashir","family":"Hassan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doaa H.","family":"Hewedi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iman","family":"Hewedi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia K.","family":"Garami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hany","family":"Al Ashwal","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nazar","family":"Zaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung-Yum","family":"Seo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vassilis","family":"Cutsuridis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergio L.","family":"Angulo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joman Y.","family":"Natesh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad M.","family":"Herzallah","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorota","family":"Frydecka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u0142a\u017cej","family":"Misiak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Salama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wael","family":"Mohamed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamad","family":"El Haj","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Hornberger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","reference":[{"key":"ref01","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1212\/WNL.0b013e3182605801","article-title":"Novel late-onset Alzheimer disease loci variants associate with brain gene expression","volume":"79","year":"2012","journal-title":"Neurology"},{"key":"ref1621","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1212\/WNL.0b013e3182605801","article-title":"Novel late-onset Alzheimer disease loci variants associate with brain gene expression","volume":"79","year":"2012","journal-title":"Neurology"},{"key":"ref2381","doi-asserted-by":"crossref","first-page":"691","DOI":"10.1212\/WNL.0000000000000154","article-title":"APOE e4 worsens hippocampal CA1 apical neuropil atrophy and episodic memory","volume":"82","year":"2014","journal-title":"Neurology"},{"key":"ref1091","doi-asserted-by":"crossref","first-page":"656","DOI":"10.1086\/342259","article-title":"Mutations in two genes encoding different subunits of a receptor signaling complex result in an identical disease phenotype","volume":"71","year":"2002","journal-title":"Am. 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