19
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Ethnoracial differences in Alzheimer’s disease from the FLorida Autopsied Multi-Ethnic (FLAME) cohort

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction:

          Our primary goal was to examine demographic and clinicopathologic differences across an ethnoracially diverse autopsy-confirmed cohort of Alzheimer’s disease cases.

          Methods:

          A retrospective study was conducted in the Florida Autopsied Multi-Ethnic cohort on 1625 Alzheimer’s disease cases, including decedents who self-reported as Hispanic/Latino (n = 67), black/African American (n = 19), and white/European American (n = 1539).

          Results:

          Hispanic decedents had a higher frequency of family history of cognitive impairment (58%), an earlier age at onset (median age of 70 years), longer disease duration (median of 12 years), and lower MMSE proximal to death (median of 4 points) compared with the other ethnoracial groups. Black decedents had a lower Braak tangle stage (stage V) and higher frequency of coexisting hippocampal sclerosis (21%); however, only hippocampal sclerosis differences survived adjustment for sex, age at onset, and disease duration. Neither Thal amyloid phase nor coexisting Lewy body disease differed across ethnoracial groups.

          Discussion:

          Despite a smaller sample size, Hispanics demonstrated longer disease duration with Alzheimer’s disease, but not greater lifespan. Neuropathologic differences across ethnoracial groups supported differences in tau pathology distribution and coexisting hippocampal sclerosis, which may impact biomarker studies.

          Related collections

          Most cited references42

          • Record: found
          • Abstract: found
          • Article: not found

          Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database.

          The past decade has witnessed hundreds of reports declaring or refuting genetic association with putative Alzheimer disease susceptibility genes. This wealth of information has become increasingly difficult to follow, much less interpret. We have created a publicly available, continuously updated database that comprehensively catalogs all genetic association studies in the field of Alzheimer disease (http://www.alzgene.org). We performed systematic meta-analyses for each polymorphism with available genotype data in at least three case-control samples. In addition to identifying the epsilon4 allele of APOE and related effects, we pinpointed over a dozen potential Alzheimer disease susceptibility genes (ACE, CHRNB2, CST3, ESR1, GAPDHS, IDE, MTHFR, NCSTN, PRNP, PSEN1, TF, TFAM and TNF) with statistically significant allelic summary odds ratios (ranging from 1.11-1.38 for risk alleles and 0.92-0.67 for protective alleles). Our database provides a powerful tool for deciphering the genetics of Alzheimer disease, and it serves as a potential model for tracking the most viable gene candidates in other genetically complex diseases.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease.

            Apolipoprotein E, type epsilon 4 allele (APOE epsilon 4), is associated with late-onset familial Alzheimer's disease (AD). There is high avidity and specific binding of amyloid beta-peptide with the protein ApoE. To test the hypothesis that late-onset familial AD may represent the clustering of sporadic AD in families large enough to be studied, we extended the analyses of APOE alleles to several series of sporadic AD patients. APOE epsilon 4 is significantly associated with a series of probable sporadic AD patients (0.36 +/- 0.042, AD, versus 0.16 +/- 0.027, controls [allele frequency estimate +/- standard error], p = 0.00031). Spouse controls did not differ from CEPH grandparent controls from the Centre d'Etude du Polymorphisme Humain (CEPH) or from literature controls. A large combined series of autopsy-documented sporadic AD patients also demonstrated highly significant association with the APOE epsilon 4 allele (0.40 +/- 0.026, p < or = 0.00001). These data support the involvement of ApoE epsilon 4 in the pathogenesis of late-onset familial and sporadic AD. ApoE isoforms may play an important role in the metabolism of beta-peptide, and APOE epsilon 4 may operate as a susceptibility gene (risk factor) for the clinical expression of AD.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The Latino mortality paradox: a test of the "salmon bias" and healthy migrant hypotheses.

              American Journal of Public Health, 89(10), 1543-1548
                Bookmark

                Author and article information

                Journal
                101231978
                33173
                Alzheimers Dement
                Alzheimers Dement
                Alzheimer's & dementia : the journal of the Alzheimer's Association
                1552-5260
                1552-5279
                18 February 2019
                18 February 2019
                May 2019
                12 May 2019
                : 15
                : 5
                : 635-643
                Affiliations
                [a ]Department of Psychiatry and Psychology, Mayo Clinic, Jacksonville, FL, USA
                [b ]Department of Neurology, Wien Center for Alzheimer’s Disease and Memory Disorders, Mount Sinai Medical Center, Miami Beach, FL, USA
                [c ]University of Florida College of Medicine, Gainesville, FL, USA
                [d ]Department of Neuroscience, Mayo Clinic, Jacksonville, FL, USA
                [e ]Department of Neurology, Mayo Clinic, Jacksonville, FL, USA
                [f ]Health Sciences Research, Mayo Clinic, Jacksonville, FL, USA
                Author notes
                [* ]Corresponding author. Tel.: 1904-953-1083; Fax: 1904-953-7117. murray.melissa@ 123456mayo.edu
                Article
                NIHMS1012926
                10.1016/j.jalz.2018.12.013
                6511501
                30792090
                ebe906a0-deb0-41fd-b4ed-6769d0fb4d66

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Article

                alzheimer disease,african american,hispanic,survival,brain,autopsy,ethnoracial

                Comments

                Comment on this article

                scite_

                Similar content261

                Cited by18

                Most referenced authors1,327