Repeat expansions in the C9ORF72 gene contribute to Alzheimer's disease in Caucasians
Abstract Recently, a hexanucleotide repeat expansion in the C9ORF72 gene has been identified to account for a significant portion of Caucasian families affected by frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Given the clinical overlap of FTD with Alzheimer's disease (...
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| Veröffentlicht in: | Neurobiology of aging 2013-05, Vol.34 (5), p.1519.e5-1519.e12 |
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| creator | Kohli, Martin A John-Williams, Krista Rajbhandary, Ruchita Naj, Adam Whitehead, Patrice Hamilton, Kara Carney, Regina M Wright, Clinton Crocco, Elizabeth Gwirtzman, Harry E Lang, Rosalyn Beecham, Gary Martin, Eden R Gilbert, John Benatar, Michael Small, Gary W Mash, Deborah Byrd, Goldie Haines, Jonathan L Pericak-Vance, Margaret A Züchner, Stephan |
| description | Abstract Recently, a hexanucleotide repeat expansion in the C9ORF72 gene has been identified to account for a significant portion of Caucasian families affected by frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Given the clinical overlap of FTD with Alzheimer's disease (AD), we hypothesized that C9ORF72 expansions might contribute to AD. In Caucasians, we found C9ORF72 expansions in the pathogenic range of FTD/ALS (>30 repeats) at a proportion of 0.76% in AD cases versus 0 in control subjects ( p = 3.3E-03; 1182 cases, 1039 controls). In contrast, no large expansions were detected in individuals of African American ethnicity (291 cases, 620 controls). However, in the range of normal variation of C9ORF72 expansions (0–23 repeat copies), we detected significant differences in distribution and mean repeat counts between Caucasians and African Americans. Clinical and pathological re-evaluation of identified C9ORF72 expansion carriers revealed 9 clinical and/or autopsy confirmed AD and 2 FTD final diagnoses. Thus, our results support the notion that large C9ORF72 expansions lead to a phenotypic spectrum of neurodegenerative disease including AD. |
| doi_str_mv | 10.1016/j.neurobiolaging.2012.10.003 |
| format | Article |
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Given the clinical overlap of FTD with Alzheimer's disease (AD), we hypothesized that C9ORF72 expansions might contribute to AD. In Caucasians, we found C9ORF72 expansions in the pathogenic range of FTD/ALS (>30 repeats) at a proportion of 0.76% in AD cases versus 0 in control subjects ( p = 3.3E-03; 1182 cases, 1039 controls). In contrast, no large expansions were detected in individuals of African American ethnicity (291 cases, 620 controls). However, in the range of normal variation of C9ORF72 expansions (0–23 repeat copies), we detected significant differences in distribution and mean repeat counts between Caucasians and African Americans. Clinical and pathological re-evaluation of identified C9ORF72 expansion carriers revealed 9 clinical and/or autopsy confirmed AD and 2 FTD final diagnoses. Thus, our results support the notion that large C9ORF72 expansions lead to a phenotypic spectrum of neurodegenerative disease including AD.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2012.10.003</identifier><identifier>PMID: 23107433</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged ; Aged, 80 and over ; Alzheimer disease ; Alzheimer Disease - ethnology ; Alzheimer Disease - genetics ; C9ORF72 ; C9orf72 Protein ; Comorbidity ; DNA Repeat Expansion - genetics ; European Continental Ancestry Group - statistics & numerical data ; Female ; Frontotemporal Dementia - ethnology ; Frontotemporal Dementia - genetics ; Genetic association ; Genetic Markers - genetics ; Genetic Predisposition to Disease - ethnology ; Genetic Predisposition to Disease - genetics ; Genetic Testing - statistics & numerical data ; Humans ; Internal Medicine ; Male ; Middle Aged ; Neurology ; Prevalence ; Proteins - genetics ; Repeat expansion ; Repeat-primed PCR ; Risk Factors ; Spectrum of neurodegenerative phenotypes ; United States - epidemiology</subject><ispartof>Neurobiology of aging, 2013-05, Vol.34 (5), p.1519.e5-1519.e12</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c561t-6236d630bcfed6a8dc933ab1d0d7c7fa5559fca637b0a7ff957e0347eb3a37523</citedby><cites>FETCH-LOGICAL-c561t-6236d630bcfed6a8dc933ab1d0d7c7fa5559fca637b0a7ff957e0347eb3a37523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197458012004939$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23107433$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kohli, Martin A</creatorcontrib><creatorcontrib>John-Williams, Krista</creatorcontrib><creatorcontrib>Rajbhandary, Ruchita</creatorcontrib><creatorcontrib>Naj, Adam</creatorcontrib><creatorcontrib>Whitehead, Patrice</creatorcontrib><creatorcontrib>Hamilton, Kara</creatorcontrib><creatorcontrib>Carney, Regina M</creatorcontrib><creatorcontrib>Wright, Clinton</creatorcontrib><creatorcontrib>Crocco, Elizabeth</creatorcontrib><creatorcontrib>Gwirtzman, Harry E</creatorcontrib><creatorcontrib>Lang, Rosalyn</creatorcontrib><creatorcontrib>Beecham, Gary</creatorcontrib><creatorcontrib>Martin, Eden R</creatorcontrib><creatorcontrib>Gilbert, John</creatorcontrib><creatorcontrib>Benatar, Michael</creatorcontrib><creatorcontrib>Small, Gary W</creatorcontrib><creatorcontrib>Mash, Deborah</creatorcontrib><creatorcontrib>Byrd, Goldie</creatorcontrib><creatorcontrib>Haines, Jonathan L</creatorcontrib><creatorcontrib>Pericak-Vance, Margaret A</creatorcontrib><creatorcontrib>Züchner, Stephan</creatorcontrib><title>Repeat expansions in the C9ORF72 gene contribute to Alzheimer's disease in Caucasians</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract Recently, a hexanucleotide repeat expansion in the C9ORF72 gene has been identified to account for a significant portion of Caucasian families affected by frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Given the clinical overlap of FTD with Alzheimer's disease (AD), we hypothesized that C9ORF72 expansions might contribute to AD. In Caucasians, we found C9ORF72 expansions in the pathogenic range of FTD/ALS (>30 repeats) at a proportion of 0.76% in AD cases versus 0 in control subjects ( p = 3.3E-03; 1182 cases, 1039 controls). In contrast, no large expansions were detected in individuals of African American ethnicity (291 cases, 620 controls). However, in the range of normal variation of C9ORF72 expansions (0–23 repeat copies), we detected significant differences in distribution and mean repeat counts between Caucasians and African Americans. Clinical and pathological re-evaluation of identified C9ORF72 expansion carriers revealed 9 clinical and/or autopsy confirmed AD and 2 FTD final diagnoses. Thus, our results support the notion that large C9ORF72 expansions lead to a phenotypic spectrum of neurodegenerative disease including AD.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer disease</subject><subject>Alzheimer Disease - ethnology</subject><subject>Alzheimer Disease - genetics</subject><subject>C9ORF72</subject><subject>C9orf72 Protein</subject><subject>Comorbidity</subject><subject>DNA Repeat Expansion - genetics</subject><subject>European Continental Ancestry Group - statistics & numerical data</subject><subject>Female</subject><subject>Frontotemporal Dementia - ethnology</subject><subject>Frontotemporal Dementia - genetics</subject><subject>Genetic association</subject><subject>Genetic Markers - genetics</subject><subject>Genetic Predisposition to Disease - ethnology</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic Testing - statistics & numerical data</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Prevalence</subject><subject>Proteins - genetics</subject><subject>Repeat expansion</subject><subject>Repeat-primed PCR</subject><subject>Risk Factors</subject><subject>Spectrum of neurodegenerative phenotypes</subject><subject>United States - epidemiology</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNklFrFDEUhYModq3-BZkHQV9mvUkmyQZEKIurQqFQ7XPIZO5ss84mazIj1l9vhq1C-9I-JXC_cy6ccwl5Q2FJgcr3u2XAKcXWx8FufdguGVBWRksA_oQsqBCrmjZaPSULoFrVjVjBCXmR8w4AVKPkc3LCOC1fzhfk6hIPaMcKfx9syD6GXPlQjddYrfXF5UaxaosBKxfDmHw7jViNsTob_lyj32N6m6vOZ7QZZ9XaTs5mX3xekme9HTK-un1PydXm0_f1l_r84vPX9dl57YSkYy0Zl53k0LoeO2lXndOc25Z20CmneiuE0L2zkqsWrOp7LRQCbxS23HIlGD8l746-hxR_TphHs_fZ4TDYgHHKhgoGfCVA64dRToVkFKQq6Icj6lLMOWFvDsnvbboxFMzcgdmZux2YuYN5Wjoo8te3m6Z2j91_8b_QC7A5Alii-eUxmew8BoedT-hG00X_2E0f7xm5wQfv7PADbzDv4pRCid9Qk5kB822-h_kcKANoNNf8L8VOtME</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Kohli, Martin A</creator><creator>John-Williams, Krista</creator><creator>Rajbhandary, Ruchita</creator><creator>Naj, Adam</creator><creator>Whitehead, Patrice</creator><creator>Hamilton, Kara</creator><creator>Carney, Regina M</creator><creator>Wright, Clinton</creator><creator>Crocco, Elizabeth</creator><creator>Gwirtzman, Harry E</creator><creator>Lang, Rosalyn</creator><creator>Beecham, Gary</creator><creator>Martin, Eden R</creator><creator>Gilbert, John</creator><creator>Benatar, Michael</creator><creator>Small, Gary W</creator><creator>Mash, Deborah</creator><creator>Byrd, Goldie</creator><creator>Haines, Jonathan L</creator><creator>Pericak-Vance, Margaret A</creator><creator>Züchner, Stephan</creator><general>Elsevier Inc</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20130501</creationdate><title>Repeat expansions in the C9ORF72 gene contribute to Alzheimer's disease in Caucasians</title><author>Kohli, Martin A ; 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Given the clinical overlap of FTD with Alzheimer's disease (AD), we hypothesized that C9ORF72 expansions might contribute to AD. In Caucasians, we found C9ORF72 expansions in the pathogenic range of FTD/ALS (>30 repeats) at a proportion of 0.76% in AD cases versus 0 in control subjects ( p = 3.3E-03; 1182 cases, 1039 controls). In contrast, no large expansions were detected in individuals of African American ethnicity (291 cases, 620 controls). However, in the range of normal variation of C9ORF72 expansions (0–23 repeat copies), we detected significant differences in distribution and mean repeat counts between Caucasians and African Americans. Clinical and pathological re-evaluation of identified C9ORF72 expansion carriers revealed 9 clinical and/or autopsy confirmed AD and 2 FTD final diagnoses. Thus, our results support the notion that large C9ORF72 expansions lead to a phenotypic spectrum of neurodegenerative disease including AD.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23107433</pmid><doi>10.1016/j.neurobiolaging.2012.10.003</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aged, 80 and over Alzheimer disease Alzheimer Disease - ethnology Alzheimer Disease - genetics C9ORF72 C9orf72 Protein Comorbidity DNA Repeat Expansion - genetics European Continental Ancestry Group - statistics & numerical data Female Frontotemporal Dementia - ethnology Frontotemporal Dementia - genetics Genetic association Genetic Markers - genetics Genetic Predisposition to Disease - ethnology Genetic Predisposition to Disease - genetics Genetic Testing - statistics & numerical data Humans Internal Medicine Male Middle Aged Neurology Prevalence Proteins - genetics Repeat expansion Repeat-primed PCR Risk Factors Spectrum of neurodegenerative phenotypes United States - epidemiology |
| title | Repeat expansions in the C9ORF72 gene contribute to Alzheimer's disease in Caucasians |
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