Neuronal gene expression correlates of Parkinson's disease with dementia
Identifieur interne : 002736 ( Main/Exploration ); précédent : 002735; suivant : 002737Neuronal gene expression correlates of Parkinson's disease with dementia
Auteurs : Chelsea Stamper [États-Unis] ; Andrew Siegel [États-Unis] ; Winnie S. Liang [États-Unis] ; John V. Pearson [États-Unis] ; Dietrich A. Stephan [États-Unis] ; Holly Shill [États-Unis] ; Don Connor [États-Unis] ; John N. Caviness [États-Unis] ; Marwan Sabbagh [États-Unis] ; Thomas G. Beach [États-Unis] ; Charles H. Adler [États-Unis] ; Travis Dunckley [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2008-08-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Capture, Dementia, Dementia (complications), Dementia (genetics), Dementia (pathology), Female, Gene Expression, Gene Expression Profiling (methods), Gene Expression Regulation (physiology), Gene expression, Humans, Laser, Male, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Nervous system diseases, Oligonucleotide Array Sequence Analysis (methods), Parkinson Disease (complications), Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson disease, Parkinson's disease, Splicing, dementia, gene expression, laser capture microdissection, mRNA splicing.
- MESH :
- chemical , genetics : Nerve Tissue Proteins.
- complications : Dementia, Parkinson Disease.
- genetics : Dementia, Parkinson Disease.
- chemical , metabolism : Nerve Tissue Proteins.
- methods : Gene Expression Profiling, Oligonucleotide Array Sequence Analysis.
- pathology : Dementia, Parkinson Disease.
- physiology : Gene Expression Regulation.
- Aged, Aged, 80 and over, Female, Gene Expression, Humans, Male.
Abstract
Dementia is a common disabling complication in patients with Parkinson's disease (PD). The underlying molecular causes of Parkinson's disease with dementia (PDD) are poorly understood. To identify candidate genes and molecular pathways involved in PDD, we have performed whole genome expression profiling of susceptible cortical neuronal populations. Results show significant differences in expression of 162 genes (P < 0.01) between PD patients who are cognitively normal (PD‐CogNL) and controls. In contrast, there were 556 genes (P < 0.01) significantly altered in PDD compared to either healthy controls or to PD‐CogNL cases. These results are consistent with increased cortical pathology in PDD relative to PD‐CogNL and identify underlying molecular changes associated with the increased pathology of PDD. Lastly, we have identified expression differences in 69 genes in PD cortical neurons that occur before the onset of dementia and that are exacerbated upon the development of dementia, suggesting that they may be relevant presymptomatic contributors to the onset of dementia in PD. These results provide new insights into the cortical molecular changes associated with PDD and provide a highly useful reference database for researchers interested in PDD. © 2008 Movement Disorder Society
Url:
- https://api.istex.fr/document/A8D91DCC85E8C6BA84CC58A9E9A21E6EA735B414/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666445
DOI: 10.1002/mds.22184
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-08-15">2008-08-15</date><biblScope unit="vol">23</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1588">1588</biblScope><biblScope unit="page" to="1595">1595</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A8D91DCC85E8C6BA84CC58A9E9A21E6EA735B414</idno><idno type="DOI">10.1002/mds.22184</idno><idno type="ArticleID">MDS22184</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Capture</term><term>Dementia</term><term>Dementia (complications)</term><term>Dementia (genetics)</term><term>Dementia (pathology)</term><term>Female</term><term>Gene Expression</term><term>Gene Expression Profiling (methods)</term><term>Gene Expression Regulation (physiology)</term><term>Gene expression</term><term>Humans</term><term>Laser</term><term>Male</term><term>Nerve Tissue Proteins (genetics)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Nervous system diseases</term><term>Oligonucleotide Array Sequence Analysis (methods)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Splicing</term><term>dementia</term><term>gene expression</term><term>laser capture microdissection</term><term>mRNA splicing</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Gene Expression Profiling</term><term>Oligonucleotide Array Sequence Analysis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Male</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Capture</term><term>Démence</term><term>Epissage</term><term>Expression génique</term><term>Laser</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dementia is a common disabling complication in patients with Parkinson's disease (PD). The underlying molecular causes of Parkinson's disease with dementia (PDD) are poorly understood. To identify candidate genes and molecular pathways involved in PDD, we have performed whole genome expression profiling of susceptible cortical neuronal populations. Results show significant differences in expression of 162 genes (P < 0.01) between PD patients who are cognitively normal (PD‐CogNL) and controls. In contrast, there were 556 genes (P < 0.01) significantly altered in PDD compared to either healthy controls or to PD‐CogNL cases. These results are consistent with increased cortical pathology in PDD relative to PD‐CogNL and identify underlying molecular changes associated with the increased pathology of PDD. Lastly, we have identified expression differences in 69 genes in PD cortical neurons that occur before the onset of dementia and that are exacerbated upon the development of dementia, suggesting that they may be relevant presymptomatic contributors to the onset of dementia in PD. These results provide new insights into the cortical molecular changes associated with PDD and provide a highly useful reference database for researchers interested in PDD. © 2008 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Arizona</li></region></list><tree><country name="États-Unis"><region name="Arizona"><name sortKey="Stamper, Chelsea" sort="Stamper, Chelsea" uniqKey="Stamper C" first="Chelsea" last="Stamper">Chelsea Stamper</name></region><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name><name sortKey="Connor, Don" sort="Connor, Don" uniqKey="Connor D" first="Don" last="Connor">Don Connor</name><name sortKey="Dunckley, Travis" sort="Dunckley, Travis" uniqKey="Dunckley T" first="Travis" last="Dunckley">Travis Dunckley</name><name sortKey="Liang, Winnie S" sort="Liang, Winnie S" uniqKey="Liang W" first="Winnie S." last="Liang">Winnie S. Liang</name><name sortKey="Pearson, John V" sort="Pearson, John V" uniqKey="Pearson J" first="John V." last="Pearson">John V. Pearson</name><name sortKey="Sabbagh, Marwan" sort="Sabbagh, Marwan" uniqKey="Sabbagh M" first="Marwan" last="Sabbagh">Marwan Sabbagh</name><name sortKey="Shill, Holly" sort="Shill, Holly" uniqKey="Shill H" first="Holly" last="Shill">Holly Shill</name><name sortKey="Siegel, Andrew" sort="Siegel, Andrew" uniqKey="Siegel A" first="Andrew" last="Siegel">Andrew Siegel</name><name sortKey="Stephan, Dietrich A" sort="Stephan, Dietrich A" uniqKey="Stephan D" first="Dietrich A." last="Stephan">Dietrich A. Stephan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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