<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lopez-Cuenca I</submitter><funding>ministerio de ciencia, innovación y universidades</funding><funding>ministerio de economía y competitividad</funding><funding>universidad complutense de madrid</funding><funding>instituto de salud carlos iii</funding><funding>ministerio de ciencia e innovación</funding><pagination>79</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9166601</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Two main genetic risks for sporadic Alzheimer's disease (AD) are a family history and ɛ4 allele of apolipoprotein E. The brain and retina are part of the central nervous system and share pathophysiological mechanisms in AD.&lt;h4>Methods&lt;/h4>We performed a cross-sectional study with 30 participants without a family history of sporadic AD (FH-) and noncarriers of ApoE ɛ4 (ApoE ɛ4-) as a control group and 34 participants with a family history of sporadic AD (FH+) and carriers of at least one ɛ4 allele (ApoE ɛ4+). We analyzed the correlations between macular volumes of retinal layers and thickness of the peripapillary retinal nerve fiber layer (pRNFL) measured by optical coherence tomography (OCT) with the brain area parameters measured by magnetic resonance imaging (MRI) in p</pubmed_abstract><journal>Alzheimer's research &amp; therapy</journal><pubmed_title>The relationship between retinal layers and brain areas in asymptomatic first-degree relatives of sporadic forms of Alzheimer's disease: an exploratory analysis.</pubmed_title><pmcid>PMC9166601</pmcid><funding_grant_id>RD16/0008/0005</funding_grant_id><funding_grant_id>PSI2015 68793-C3-1-R</funding_grant_id><funding_grant_id>CT82/20-CT83/20</funding_grant_id><funding_grant_id>FPU17/01023</funding_grant_id><funding_grant_id>RED2018-102499-T</funding_grant_id><funding_grant_id>CT42/18-CT43/18</funding_grant_id><pubmed_authors>Gil P</pubmed_authors><pubmed_authors>Barabash A</pubmed_authors><pubmed_authors>Marcos-Dolado A</pubmed_authors><pubmed_authors>Elvira-Hurtado L</pubmed_authors><pubmed_authors>Salazar JJ</pubmed_authors><pubmed_authors>Sanchez-Puebla L</pubmed_authors><pubmed_authors>Ramirez-Torano F</pubmed_authors><pubmed_authors>Yus-Fuertes M</pubmed_authors><pubmed_authors>Arrazola-Garcia J</pubmed_authors><pubmed_authors>Gil-Martinez L</pubmed_authors><pubmed_authors>Lopez-Cuenca I</pubmed_authors><pubmed_authors>Salobrar-Garcia E</pubmed_authors><pubmed_authors>Ramirez JM</pubmed_authors><pubmed_authors>Fernandez-Albarral JA</pubmed_authors><pubmed_authors>de Hoz R</pubmed_authors><pubmed_authors>Fuentes-Ferrer ME</pubmed_authors><pubmed_authors>Ramirez AI</pubmed_authors></additional><is_claimable>false</is_claimable><name>The relationship between retinal layers and brain areas in asymptomatic first-degree relatives of sporadic forms of Alzheimer's disease: an exploratory analysis.</name><description>&lt;h4>Background&lt;/h4>Two main genetic risks for sporadic Alzheimer's disease (AD) are a family history and ɛ4 allele of apolipoprotein E. The brain and retina are part of the central nervous system and share pathophysiological mechanisms in AD.&lt;h4>Methods&lt;/h4>We performed a cross-sectional study with 30 participants without a family history of sporadic AD (FH-) and noncarriers of ApoE ɛ4 (ApoE ɛ4-) as a control group and 34 participants with a family history of sporadic AD (FH+) and carriers of at least one ɛ4 allele (ApoE ɛ4+). We analyzed the correlations between macular volumes of retinal layers and thickness of the peripapillary retinal nerve fiber layer (pRNFL) measured by optical coherence tomography (OCT) with the brain area parameters measured by magnetic resonance imaging (MRI) in p</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2026-05-09T18:59:27.942Z</modification><creation>2024-11-13T17:41:18.881Z</creation></dates><accession>S-EPMC9166601</accession><cross_references><pubmed>35659054</pubmed><doi>10.1186/s13195-022-01008-5</doi></cross_references></HashMap>