What Can Biomarkers Tell Us About Cognition in Parkinson's Disease?
Identifieur interne : 000359 ( Main/Exploration ); précédent : 000358; suivant : 000360What Can Biomarkers Tell Us About Cognition in Parkinson's Disease?
Auteurs : Brit Mollenhauer [Allemagne] ; Lynn Rochester [Royaume-Uni] ; Alice Chen-Plotkin [États-Unis] ; David Brooks [Royaume-Uni, Danemark]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Biological Markers (metabolism), Cognition (physiology), Cognition Disorders (diagnosis), Cognition Disorders (genetics), Cognition Disorders (metabolism), Genetic Variation (genetics), Humans, Parkinson Disease (complications), Parkinson Disease (diagnosis), Parkinson Disease (genetics), Parkinson Disease (metabolism), Risk.
- MESH :
- chemical , metabolism : Biological Markers.
- complications : Parkinson Disease.
- diagnosis : Cognition Disorders, Parkinson Disease.
- genetics : Cognition Disorders, Genetic Variation, Parkinson Disease.
- metabolism : Cognition Disorders, Parkinson Disease.
- physiology : Cognition.
- Animals, Humans, Risk.
Abstract
Cognitive decline is common in Parkinson's disease (PD), even in the early motor stage, and this non-motor feature impacts quality of life and prognosis tremendously. In this article, we discuss marker candidates for cognitive decline in PD from different angles, including functional and structural imaging techniques, biological fluid markers in cerebrospinal fluid, and blood genetic predictors, as well as gait as a surrogate marker of cognitive decline. Specifically, imaging-based markers of cognitive impairment in PD include cortical atrophy, reduced cortical metabolism, loss of cortical cholinergic and frontal dopaminergic function, as well as an increased cortical amyloid load. Reduced β-amyloid(1-42) in cerebrospinal fluid and lower plasma levels of epidermal growth factor are predictors for cognitive decline in PD. In addition, genetic variation in the apolipoprotein E (
Url:
DOI: 10.1002/mds.25846
PubMed: 24757111
PubMed Central: 4384332
Affiliations:
- Allemagne, Danemark, Royaume-Uni, États-Unis
- Angleterre, Basse-Saxe, Grand Londres, Pennsylvanie
- Göttingen, Londres
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Le document en format XML
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Hammersmith Hospital, London, United Kingdom</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Medicine, Imperial College London. Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="A5">Department of Nuclear Medicine, Aarhus University, Nïrrebrogade, Aarhus, Denmark</nlm:aff><country xml:lang="fr">Danemark</country><wicri:regionArea>Department of Nuclear Medicine, Aarhus University, Nïrrebrogade, Aarhus</wicri:regionArea><wicri:noRegion>Aarhus</wicri:noRegion></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Markers (metabolism)</term><term>Cognition (physiology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (genetics)</term><term>Cognition Disorders (metabolism)</term><term>Genetic Variation (genetics)</term><term>Humans</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Risk</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biological Markers</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cognition Disorders</term><term>Genetic Variation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cognition</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Risk</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Cognitive decline is common in Parkinson's disease (PD), even in the early motor stage, and this non-motor feature impacts quality of life and prognosis tremendously. In this article, we discuss marker candidates for cognitive decline in PD from different angles, including functional and structural imaging techniques, biological fluid markers in cerebrospinal fluid, and blood genetic predictors, as well as gait as a surrogate marker of cognitive decline. Specifically, imaging-based markers of cognitive impairment in PD include cortical atrophy, reduced cortical metabolism, loss of cortical cholinergic and frontal dopaminergic function, as well as an increased cortical amyloid load. Reduced β-amyloid(1-42) in cerebrospinal fluid and lower plasma levels of epidermal growth factor are predictors for cognitive decline in PD. In addition, genetic variation in the apolipoprotein E (<italic>APOE</italic>), catechol-O-methyltransferase (<italic>COMT</italic>), microtubule-associated protein tau (<italic>MAPT</italic>), and glucocerebrosidase (<italic>GBA</italic>) genes may confer risk for cognitive impairment in PD; and gait disturbance may also indicate an increased risk for dementia. Other marker candidates have been proposed and are discussed. All of the current studies are hampered by gaps in our knowledge about the molecular causes of cognitive decline, which will have to be considered in future biomarker studies.</p></div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Danemark</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Basse-Saxe</li><li>Grand Londres</li><li>Pennsylvanie</li></region><settlement><li>Göttingen</li><li>Londres</li></settlement></list><tree><country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Mollenhauer, Brit" sort="Mollenhauer, Brit" uniqKey="Mollenhauer B" first="Brit" last="Mollenhauer">Brit Mollenhauer</name></region></country><country name="Royaume-Uni"><noRegion><name sortKey="Rochester, Lynn" sort="Rochester, Lynn" uniqKey="Rochester L" first="Lynn" last="Rochester">Lynn Rochester</name></noRegion><name sortKey="Brooks, David" sort="Brooks, David" uniqKey="Brooks D" first="David" last="Brooks">David Brooks</name></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Chen Plotkin, Alice" sort="Chen Plotkin, Alice" uniqKey="Chen Plotkin A" first="Alice" last="Chen-Plotkin">Alice Chen-Plotkin</name></region></country><country name="Danemark"><noRegion><name sortKey="Brooks, David" sort="Brooks, David" uniqKey="Brooks D" first="David" last="Brooks">David Brooks</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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