Evidence for an association between KIBRA and late-onset Alzheimer's disease
We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibil...
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| Published in | Neurobiology of aging Vol. 31; no. 6; pp. 901 - 909 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Elsevier Inc
01.06.2010
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (P<0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (P=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (P=0.039; OR=1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD. |
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| AbstractList | We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the
KIBRA
gene,
KIBRA
rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer’s disease (AD), we investigated the possibility of an association between the
KIBRA
gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests.
KIBRA
was significantly over-expressed and 3 of its 4 known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (p<0.010, corrected) in a study of laser capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for
KIBRA
rs17070145,
KIBRA
T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the
KIBRA
rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (p=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (p=0.039; OR=1.26). Our findings suggest that
KIBRA
is associated with both individual variation in normal episodic memory and predisposition to AD. We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (P<0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (P=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (P=0.039; OR=1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD. Abstract We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions ( P < 0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions ( P < 0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects ( P = 0.034; OR = 1.29) and in a combined analysis of 1026 additional living and expired subjects ( P = 0.039; OR = 1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD. We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (P<0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (P=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (P=0.039; OR=1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD.We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA rs17070145 (T-allele). Since memory impairment is a cardinal clinical feature of Alzheimer's disease (AD), we investigated the possibility of an association between the KIBRA gene and AD using data from neuronal gene expression, brain imaging studies, and genetic association tests. KIBRA was significantly over-expressed and three of its four known binding partners under-expressed in AD-affected hippocampal, posterior cingulate and temporal cortex regions (P<0.010, corrected) in a study of laser-capture microdissected neurons. Using positron emission tomography in a cohort of cognitively normal, late-middle-aged persons genotyped for KIBRA rs17070145, KIBRA T non-carriers exhibited lower glucose metabolism than did carriers in posterior cingulate and precuneus brain regions (P<0.001, uncorrected). Lastly, non-carriers of the KIBRA rs17070145 T-allele had increased risk of late-onset AD in an association study of 702 neuropathologically verified expired subjects (P=0.034; OR=1.29) and in a combined analysis of 1026 additional living and expired subjects (P=0.039; OR=1.26). Our findings suggest that KIBRA is associated with both individual variation in normal episodic memory and predisposition to AD. |
| Author | Corneveaux, Jason J. Grover, Andrew Bandy, Daniel Craig, David W. Coon, Keith D. Alexander, Gene E. Rogers, Joseph Hutton, Michael L. Papassotiropoulos, Andreas Chen, Kewei Liang, Winnie S. Hu-Lince, Diane Aasly, Jan O. Reiman, Eric M. Myers, Amanda J. Heun, Reinhard Mastroeni, Diego Sando, Sigrid B. Joshipura, Keta D. Ravid, Rivka Zismann, Victoria L. Kölsch, Heike Pearson, John V. Jessen, Frank Stephan, Dietrich A. Webster, Jennifer A. Petersen, Ron C. Beach, Thomas G. Huentelman, Matthew J. Caselli, Richard J. Dunckley, Travis Melquist, Stacey Lee, Wendy |
| AuthorAffiliation | b Arizona Alzheimer’s Consortium, 901 E. Willetta Street, Phoenix AZ 85006, U.S.A o Mayo Clinic, Department of Neuroscience, 4500 San Pablo Road, Jacksonville, FL 32224, U.S.A j Arizona State University, Department of Mathematics, PO Box 871804, Tempe, AZ 85287, U.S.A l Department of Neurology, St. Olav’s Hospital, Edvard Griegs gate 8, 7006 Trondheim, Norway k Dutch Royal Academy of Arts and Sciences, Netherlands Institute for Neurosciences, Meibergdreef 47 AB Amsterdam, Netherlands r Mayo Clinic, Department of Neurology, 13400 E. Shea Boulevard, Scottsdale, AZ 85259, U.S.A a Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ, 85004, U.S.A s University of Basel, Division of Molecular Psychology and Life Sciences Training Facility, Biozentrum, Basel, Switzerland m Department of Neuroscience, Norwegian University of Science and Technology, NTNU, 7491 Trondheim, Norway d University of Arizona, Department of Psychiatry, 1501 N. Campbell Avenu |
| AuthorAffiliation_xml | – name: q University of Arizona, Department of Psychology and Evelyn F. McKnight Brain Institute, 1503 E. University, Tucson, AZ 85721, U.S.A – name: g Center for Thoracic Disease, The Heart and Lung Institute, St. Joseph’s Hospital, 500 West Thomas Rd., Suite 500, Phoenix, AZ 85013, U.S.A – name: s University of Basel, Division of Molecular Psychology and Life Sciences Training Facility, Biozentrum, Basel, Switzerland – name: c Banner Alzheimer’s Institute, 901 E. Willetta Street, Phoenix, AZ 85006, U.S.A – name: o Mayo Clinic, Department of Neuroscience, 4500 San Pablo Road, Jacksonville, FL 32224, U.S.A – name: i University of Arizona, Department of Radiology, 1501 N. Campbell Avenue, PO Box 245002, Tucson, AZ 85724, U.S.A – name: l Department of Neurology, St. Olav’s Hospital, Edvard Griegs gate 8, 7006 Trondheim, Norway – name: f National Institute on Aging, National Institutes of Health, Laboratory of Neurogenetics, Building 31, Room 5C27, 31 Center Drive, MSC 2292, Bethesda, MD, 20892, U.S.A – name: a Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ, 85004, U.S.A – name: e University of Miami, Miller School of Medicine, Department of Psychiatry and Behavioral Sciences, 1695 N.W. 9 th Avenue, PO Box 016960 (D-29), Miami, FL 33101, U.S.A – name: p Mayo Clinic, Department of Neurology, 200 First Street S.W., Rochester, MN 55905, U.S.A – name: n Department of Psychiatry, University of Bonn, Bonn, Germany – name: j Arizona State University, Department of Mathematics, PO Box 871804, Tempe, AZ 85287, U.S.A – name: m Department of Neuroscience, Norwegian University of Science and Technology, NTNU, 7491 Trondheim, Norway – name: d University of Arizona, Department of Psychiatry, 1501 N. Campbell Avenue, PO Box 245002, Tucson, AZ 85724, U.S.A – name: b Arizona Alzheimer’s Consortium, 901 E. Willetta Street, Phoenix AZ 85006, U.S.A – name: h Sun Health Research Institute, 10515 W. Santa Fe Drive, Sun City, AZ 85351, U.S.A – name: r Mayo Clinic, Department of Neurology, 13400 E. Shea Boulevard, Scottsdale, AZ 85259, U.S.A – name: k Dutch Royal Academy of Arts and Sciences, Netherlands Institute for Neurosciences, Meibergdreef 47 AB Amsterdam, Netherlands |
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Fifth Street, Phoenix, AZ 85004, USA – sequence: 5 givenname: Amanda J. surname: Myers fullname: Myers, Amanda J. organization: University of Miami, Miller School of Medicine, Department of Psychiatry and Behavioral Sciences, 1695 N.W. 9th Avenue, PO Box 016960 (D-29), Miami, FL 33101, USA – sequence: 6 givenname: Victoria L. surname: Zismann fullname: Zismann, Victoria L. organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ 85004, USA – sequence: 7 givenname: Keta D. surname: Joshipura fullname: Joshipura, Keta D. organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ 85004, USA – sequence: 8 givenname: John V. surname: Pearson fullname: Pearson, John V. organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. 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Willetta Street, Phoenix, AZ 85006, USA – sequence: 19 givenname: Rivka surname: Ravid fullname: Ravid, Rivka organization: Dutch Royal Academy of Arts and Sciences, Netherlands Institute for Neurosciences, Meibergdreef 47 AB, Amsterdam, The Netherlands – sequence: 20 givenname: Sigrid B. surname: Sando fullname: Sando, Sigrid B. organization: Department of Neurology, St. Olav's Hospital, Edvard Griegs Gate 8, 7006 Trondheim, Norway – sequence: 21 givenname: Jan O. surname: Aasly fullname: Aasly, Jan O. organization: Department of Neurology, St. Olav's Hospital, Edvard Griegs Gate 8, 7006 Trondheim, Norway – sequence: 22 givenname: Reinhard surname: Heun fullname: Heun, Reinhard organization: Department of Psychiatry, University of Bonn, Bonn, Germany – sequence: 23 givenname: Frank surname: Jessen fullname: Jessen, Frank organization: Department of Psychiatry, University of Bonn, Bonn, Germany – sequence: 24 givenname: Heike surname: Kölsch fullname: Kölsch, Heike organization: Department of Psychiatry, University of Bonn, Bonn, Germany – sequence: 25 givenname: Joseph surname: Rogers fullname: Rogers, Joseph organization: Arizona Alzheimer's Consortium, 901 E. 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Willetta Street, Phoenix, AZ 85006, USA – sequence: 31 givenname: Andreas surname: Papassotiropoulos fullname: Papassotiropoulos, Andreas organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ 85004, USA – sequence: 32 givenname: Dietrich A. surname: Stephan fullname: Stephan, Dietrich A. organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ 85004, USA – sequence: 33 givenname: Matthew J. surname: Huentelman fullname: Huentelman, Matthew J. email: mhuentelman@tgen.org organization: Translational Genomics Research Institute (TGen), Neurogenomics Division, 445 N. Fifth Street, Phoenix, AZ 85004, USA |
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| Copyright | 2008 Elsevier Inc. Elsevier Inc. 2015 INIST-CNRS Copyright 2008 Elsevier Inc. All rights reserved. 2010 Elsevier Inc. All rights reserved. 2010 |
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| Issue | 6 |
| Keywords | Genetics Expression profiling Imaging Memory Nervous system diseases Senescence Alzheimer disease Central nervous system disease Degenerative disease Cerebral disorder |
| Language | English |
| License | https://www.elsevier.com/tdm/userlicense/1.0 CC BY 4.0 Copyright 2008 Elsevier Inc. All rights reserved. |
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| Snippet | We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA... Abstract We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA... We recently reported evidence for an association between the individual variation in normal human episodic memory and a common variant of the KIBRA gene, KIBRA... |
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| SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - complications Alzheimer Disease - diagnostic imaging Alzheimer Disease - genetics Alzheimer Disease - pathology Apolipoproteins E - genetics Biological and medical sciences Brain - diagnostic imaging Brain - enzymology Brain - pathology Brain Mapping Cognition Disorders - etiology Cognition Disorders - genetics Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Development. Senescence. Regeneration. Transplantation Expression profiling Female Fundamental and applied biological sciences. Psychology Gene Expression Profiling - methods Genetic Predisposition to Disease Genetics Genome-Wide Association Study - methods Genotype Glial Fibrillary Acidic Protein - metabolism Humans Imaging Internal Medicine Intracellular Signaling Peptides and Proteins Male Medical sciences Memory Neurology Neurons - metabolism Neurons - pathology Neuropsychological Tests Oligonucleotide Array Sequence Analysis - methods Phosphoproteins Polymorphism, Single Nucleotide - genetics Positron-Emission Tomography - methods Proteins - genetics Vertebrates: nervous system and sense organs |
| Title | Evidence for an association between KIBRA and late-onset Alzheimer's disease |
| URI | https://www.clinicalkey.com/#!/content/1-s2.0-S0197458008002583 https://www.clinicalkey.es/playcontent/1-s2.0-S0197458008002583 https://dx.doi.org/10.1016/j.neurobiolaging.2008.07.014 https://www.ncbi.nlm.nih.gov/pubmed/18789830 https://www.proquest.com/docview/733901622 https://pubmed.ncbi.nlm.nih.gov/PMC2913703 |
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