An anemia of Alzheimer's disease
Lower hemoglobin is associated with cognitive impairment and Alzheimer's disease (AD). Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifest...
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| Veröffentlicht in: | Molecular psychiatry 2014-11, Vol.19 (11), p.1227-1234 |
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| container_title | Molecular psychiatry |
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| creator | Faux, N G Rembach, A Wiley, J Ellis, K A Ames, D Fowler, C J Martins, R N Pertile, K K Rumble, R L Trounson, B Masters, C L Bush, A I |
| description | Lower hemoglobin is associated with cognitive impairment and Alzheimer's disease (AD). Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifestyle (AIBL) study (a community-based, cross-sectional cohort comprising 768 healthy controls (HC), 133 participants with mild cognitive impairment (MCI) and 211 participants with AD). We found that individuals with AD had significantly lower hemoglobin, mean cell hemoglobin concentrations, packed cell volume and higher erythrocyte sedimentation rates (adjusted for age, gender, APOE-ɛ4 and site). In AD, plasma iron, transferrin, transferrin saturation and red cell folate levels exhibited a significant distortion of their customary relationship to hemoglobin levels. There was a strong association between anemia and AD (adjusted odds ratio (OR)=2.43, confidence interval (CI) (1.31, 4.54)). Moreover, AD emerged as a strong risk factor for anemia on step-down regression, even when controlling for all other available explanations for anemia (adjusted OR=3.41, 95% CI (1.68, 6.92)). These data indicated that AD is complicated by anemia, which may itself contribute to cognitive decline. |
| doi_str_mv | 10.1038/mp.2013.178 |
| format | Article |
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Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifestyle (AIBL) study (a community-based, cross-sectional cohort comprising 768 healthy controls (HC), 133 participants with mild cognitive impairment (MCI) and 211 participants with AD). We found that individuals with AD had significantly lower hemoglobin, mean cell hemoglobin concentrations, packed cell volume and higher erythrocyte sedimentation rates (adjusted for age, gender, APOE-ɛ4 and site). In AD, plasma iron, transferrin, transferrin saturation and red cell folate levels exhibited a significant distortion of their customary relationship to hemoglobin levels. There was a strong association between anemia and AD (adjusted odds ratio (OR)=2.43, confidence interval (CI) (1.31, 4.54)). Moreover, AD emerged as a strong risk factor for anemia on step-down regression, even when controlling for all other available explanations for anemia (adjusted OR=3.41, 95% CI (1.68, 6.92)). These data indicated that AD is complicated by anemia, which may itself contribute to cognitive decline.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/mp.2013.178</identifier><identifier>PMID: 24419041</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/699/1541/13 ; 692/699/375/365/1283 ; Aged ; Aged, 80 and over ; Alzheimer Disease - blood ; Alzheimer Disease - complications ; Alzheimer's disease ; Anemia ; Anemia - blood ; Anemia - complications ; Apolipoprotein E ; Australia - epidemiology ; Behavioral Sciences ; Biological Psychology ; Cell size ; Cognitive ability ; Cognitive Dysfunction - blood ; Cognitive Dysfunction - complications ; Complications and side effects ; Cross-Sectional Studies ; Development and progression ; Erythrocyte sedimentation rate ; Female ; Folic acid ; Folic Acid - blood ; Hemoglobin ; Hemoglobins - metabolism ; Homeostasis ; Humans ; Iron ; Iron - blood ; Male ; Measurement ; Medicine ; Medicine & Public Health ; Middle Aged ; Neurodegenerative diseases ; Neuroimaging ; Neurosciences ; original-article ; Pharmacotherapy ; Prospective Studies ; Psychiatry ; Risk Factors ; Transferrin - metabolism ; Transferrins</subject><ispartof>Molecular psychiatry, 2014-11, Vol.19 (11), p.1227-1234</ispartof><rights>Macmillan Publishers Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 2014</rights><rights>Macmillan Publishers Limited 2014.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c519t-f75b631f807ccbac6c2977f6662e2c8053c46f191dc7214736c0249f1d455b63</citedby><cites>FETCH-LOGICAL-c519t-f75b631f807ccbac6c2977f6662e2c8053c46f191dc7214736c0249f1d455b63</cites><orcidid>0000-0003-4594-8818 ; 0000000345948818</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/mp.2013.178$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/mp.2013.178$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24419041$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Faux, N G</creatorcontrib><creatorcontrib>Rembach, A</creatorcontrib><creatorcontrib>Wiley, J</creatorcontrib><creatorcontrib>Ellis, K A</creatorcontrib><creatorcontrib>Ames, D</creatorcontrib><creatorcontrib>Fowler, C J</creatorcontrib><creatorcontrib>Martins, R N</creatorcontrib><creatorcontrib>Pertile, K K</creatorcontrib><creatorcontrib>Rumble, R L</creatorcontrib><creatorcontrib>Trounson, B</creatorcontrib><creatorcontrib>Masters, C L</creatorcontrib><creatorcontrib>Bush, A I</creatorcontrib><creatorcontrib>AIBL Research Group</creatorcontrib><creatorcontrib>The AIBL Research Group</creatorcontrib><title>An anemia of Alzheimer's disease</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>Lower hemoglobin is associated with cognitive impairment and Alzheimer's disease (AD). Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifestyle (AIBL) study (a community-based, cross-sectional cohort comprising 768 healthy controls (HC), 133 participants with mild cognitive impairment (MCI) and 211 participants with AD). We found that individuals with AD had significantly lower hemoglobin, mean cell hemoglobin concentrations, packed cell volume and higher erythrocyte sedimentation rates (adjusted for age, gender, APOE-ɛ4 and site). In AD, plasma iron, transferrin, transferrin saturation and red cell folate levels exhibited a significant distortion of their customary relationship to hemoglobin levels. There was a strong association between anemia and AD (adjusted odds ratio (OR)=2.43, confidence interval (CI) (1.31, 4.54)). Moreover, AD emerged as a strong risk factor for anemia on step-down regression, even when controlling for all other available explanations for anemia (adjusted OR=3.41, 95% CI (1.68, 6.92)). These data indicated that AD is complicated by anemia, which may itself contribute to cognitive decline.</description><subject>692/699/1541/13</subject><subject>692/699/375/365/1283</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - blood</subject><subject>Alzheimer Disease - complications</subject><subject>Alzheimer's disease</subject><subject>Anemia</subject><subject>Anemia - blood</subject><subject>Anemia - complications</subject><subject>Apolipoprotein E</subject><subject>Australia - epidemiology</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Cell size</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction - blood</subject><subject>Cognitive Dysfunction - complications</subject><subject>Complications and side effects</subject><subject>Cross-Sectional Studies</subject><subject>Development and progression</subject><subject>Erythrocyte sedimentation rate</subject><subject>Female</subject><subject>Folic acid</subject><subject>Folic Acid - blood</subject><subject>Hemoglobin</subject><subject>Hemoglobins - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Iron</subject><subject>Iron - blood</subject><subject>Male</subject><subject>Measurement</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neurodegenerative diseases</subject><subject>Neuroimaging</subject><subject>Neurosciences</subject><subject>original-article</subject><subject>Pharmacotherapy</subject><subject>Prospective Studies</subject><subject>Psychiatry</subject><subject>Risk Factors</subject><subject>Transferrin - metabolism</subject><subject>Transferrins</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkUtLAzEUhYMotlZX7mXAhYJOzc17lqX4goKb7sM0k9Qp86hJu9Bfb4ZWqVJEskjI_e65j4PQOeAhYKru6uWQYKBDkOoA9YFJkXIu1WF8U56lDBTroZMQFhh3QX6MeoQxyDCDPkpGTZI3ti7zpHXJqPp4tWVt_VVIijLYPNhTdOTyKtiz7T1A04f76fgpnbw8Po9Hk9RwyFapk3wmKDiFpTGz3AhDMimdEIJYYhTm1DDhIIPCSBLboMJgwjIHBeNd5gBdb2SXvn1b27DSdRmMrarYXLsOGoRgBAuO6T9QUMAZizsZoMtf6KJd-ybOoYlgXEoKRP1FRS3BBFFsh5rnldVl49qVz01XWo-oUlzwTHYVh3uoeIq4Y9M21pXx_0fCzSbB-DYEb51e-rLO_bsGrDt_db3Unb86-hvpi22r61lti2_2y9AI3G6AEEPN3PqdWfbofQIiQKdr</recordid><startdate>20141101</startdate><enddate>20141101</enddate><creator>Faux, N G</creator><creator>Rembach, A</creator><creator>Wiley, J</creator><creator>Ellis, K A</creator><creator>Ames, D</creator><creator>Fowler, C J</creator><creator>Martins, R N</creator><creator>Pertile, K K</creator><creator>Rumble, R L</creator><creator>Trounson, B</creator><creator>Masters, C L</creator><creator>Bush, A I</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-4594-8818</orcidid><orcidid>https://orcid.org/0000000345948818</orcidid></search><sort><creationdate>20141101</creationdate><title>An anemia of Alzheimer's disease</title><author>Faux, N G ; Rembach, A ; Wiley, J ; Ellis, K A ; Ames, D ; Fowler, C J ; Martins, R N ; Pertile, K K ; Rumble, R L ; Trounson, B ; Masters, C L ; Bush, A I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c519t-f75b631f807ccbac6c2977f6662e2c8053c46f191dc7214736c0249f1d455b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>692/699/1541/13</topic><topic>692/699/375/365/1283</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - 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Academic</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Faux, N G</au><au>Rembach, A</au><au>Wiley, J</au><au>Ellis, K A</au><au>Ames, D</au><au>Fowler, C J</au><au>Martins, R N</au><au>Pertile, K K</au><au>Rumble, R L</au><au>Trounson, B</au><au>Masters, C L</au><au>Bush, A I</au><aucorp>AIBL Research Group</aucorp><aucorp>The AIBL Research Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An anemia of Alzheimer's disease</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>19</volume><issue>11</issue><spage>1227</spage><epage>1234</epage><pages>1227-1234</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>Lower hemoglobin is associated with cognitive impairment and Alzheimer's disease (AD). Since brain iron homeostasis is perturbed in AD, we investigated whether this is peripherally reflected in the hematological and related blood chemistry values from the Australian Imaging Biomarker and Lifestyle (AIBL) study (a community-based, cross-sectional cohort comprising 768 healthy controls (HC), 133 participants with mild cognitive impairment (MCI) and 211 participants with AD). We found that individuals with AD had significantly lower hemoglobin, mean cell hemoglobin concentrations, packed cell volume and higher erythrocyte sedimentation rates (adjusted for age, gender, APOE-ɛ4 and site). In AD, plasma iron, transferrin, transferrin saturation and red cell folate levels exhibited a significant distortion of their customary relationship to hemoglobin levels. There was a strong association between anemia and AD (adjusted odds ratio (OR)=2.43, confidence interval (CI) (1.31, 4.54)). Moreover, AD emerged as a strong risk factor for anemia on step-down regression, even when controlling for all other available explanations for anemia (adjusted OR=3.41, 95% CI (1.68, 6.92)). These data indicated that AD is complicated by anemia, which may itself contribute to cognitive decline.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24419041</pmid><doi>10.1038/mp.2013.178</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-4594-8818</orcidid><orcidid>https://orcid.org/0000000345948818</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 692/699/1541/13 692/699/375/365/1283 Aged Aged, 80 and over Alzheimer Disease - blood Alzheimer Disease - complications Alzheimer's disease Anemia Anemia - blood Anemia - complications Apolipoprotein E Australia - epidemiology Behavioral Sciences Biological Psychology Cell size Cognitive ability Cognitive Dysfunction - blood Cognitive Dysfunction - complications Complications and side effects Cross-Sectional Studies Development and progression Erythrocyte sedimentation rate Female Folic acid Folic Acid - blood Hemoglobin Hemoglobins - metabolism Homeostasis Humans Iron Iron - blood Male Measurement Medicine Medicine & Public Health Middle Aged Neurodegenerative diseases Neuroimaging Neurosciences original-article Pharmacotherapy Prospective Studies Psychiatry Risk Factors Transferrin - metabolism Transferrins |
| title | An anemia of Alzheimer's disease |
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