Accumulation of amyloid-β in the cerebellar cortex of essential tremor patients.
Identifieur interne : 000593 ( PubMed/Checkpoint ); précédent : 000592; suivant : 000594Accumulation of amyloid-β in the cerebellar cortex of essential tremor patients.
Auteurs : Eric Béliveau [Canada] ; Cyntia Tremblay [Canada] ; Émilie Aubry-Lafontaine [Canada] ; Sarah Paris-Robidas [Canada] ; Charlotte Delay [Canada] ; Chris Robinson [Canada] ; Les Ferguson [Canada] ; Ali H. Rajput [Canada] ; Alex Rajput [Canada] ; Frédéric Calon [Canada]Source :
- Neurobiology of disease [ 1095-953X ] ; 2015.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Alzheimer Disease (metabolism), Amyloid beta-Peptides (metabolism), Amyloid beta-Protein Precursor (metabolism), Apolipoprotein E4 (metabolism), Cerebellar Cortex (metabolism), Essential Tremor (metabolism), Female, Humans, Male, Membrane Proteins (metabolism), Nerve Tissue Proteins (metabolism), Neurofilament Proteins (metabolism), Parietal Lobe (metabolism), Parkinson Disease (metabolism), Peptide Fragments (metabolism), Phosphorylation, Purkinje Cells (metabolism), Temporal Lobe (metabolism), tau Proteins (metabolism).
- MESH :
- chemical , metabolism : Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Apolipoprotein E4, Membrane Proteins, Nerve Tissue Proteins, Neurofilament Proteins, Peptide Fragments, tau Proteins.
- metabolism : Alzheimer Disease, Cerebellar Cortex, Essential Tremor, Parietal Lobe, Parkinson Disease, Purkinje Cells, Temporal Lobe.
- Aged, Aged, 80 and over, Female, Humans, Male, Phosphorylation.
Abstract
The accumulation of insoluble amyloid-beta (Aβ) peptides is associated with neurodegenerative disorders, such as Alzheimer's disease (AD). As essential tremor (ET) could involve neurodegenerative processes in the cerebellum, we quantified soluble and insoluble Aβ in cerebellar cortices from patients diagnosed with ET (n=9), compared to Controls (n=16) or individuals with Parkinson's disease (n=10). Although ante-mortem cognitive performance was not documented, all individuals included had the diagnosis of AD ruled out by a neuropathologist. ELISA-determined concentrations of insoluble Aβ42 in ET patients displayed a bimodal distribution, with a median 246-fold higher than in Controls (P<0.01, Kruskal-Wallis). Higher Aβ42 concentrations were measured in the parietal cortex of the same ET patients, compared to Controls (107-fold median increase, P<0.01, Kruskal-Wallis), but similar phosphorylated tau levels were detected. The rise in cerebellar insoluble Aβ42 concentrations is not associated to APP expression and processing or the ApoE4 status. However, Aβ42 levels in ET individuals were correlated with cerebellar insoluble phosphorylated tau (r(2)=0.71, P=0.005), unphosphorylated neurofilament heavy chain (NF-H; r(2)=0.50, P=0.030) and Lingo-1 (r(2)=0.73, P=0.007), indicative of a generalized neurodegenerative process involving the cerebellum. Our results suggest prevalent accumulations of insoluble Aβ42 in the cerebellum of ET, but not in age-matched PD. Whether this anomaly plays a role in ET symptoms warrants further investigations.
DOI: 10.1016/j.nbd.2015.07.016
PubMed: 26253607
Affiliations:
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Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author><author><name sortKey="Tremblay, Cyntia" sort="Tremblay, Cyntia" uniqKey="Tremblay C" first="Cyntia" last="Tremblay">Cyntia Tremblay</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author><author><name sortKey="Aubry Lafontaine, Emilie" sort="Aubry Lafontaine, Emilie" uniqKey="Aubry Lafontaine E" first="Émilie" last="Aubry-Lafontaine">Émilie Aubry-Lafontaine</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author><author><name sortKey="Paris Robidas, Sarah" sort="Paris Robidas, Sarah" uniqKey="Paris Robidas S" first="Sarah" last="Paris-Robidas">Sarah Paris-Robidas</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author><author><name sortKey="Delay, Charlotte" sort="Delay, Charlotte" uniqKey="Delay C" first="Charlotte" last="Delay">Charlotte Delay</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author><author><name sortKey="Robinson, Chris" sort="Robinson, Chris" uniqKey="Robinson C" first="Chris" last="Robinson">Chris Robinson</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK</wicri:regionArea><wicri:noRegion>SK</wicri:noRegion></affiliation></author><author><name sortKey="Ferguson, Les" sort="Ferguson, Les" uniqKey="Ferguson L" first="Les" last="Ferguson">Les Ferguson</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK</wicri:regionArea><wicri:noRegion>SK</wicri:noRegion></affiliation></author><author><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H" last="Rajput">Ali H. Rajput</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK</wicri:regionArea><wicri:noRegion>SK</wicri:noRegion></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK</wicri:regionArea><wicri:noRegion>SK</wicri:noRegion></affiliation></author><author><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada. Electronic address: frederic.calon@crchul.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC</wicri:regionArea><wicri:noRegion>QC</wicri:noRegion></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer Disease (metabolism)</term><term>Amyloid beta-Peptides (metabolism)</term><term>Amyloid beta-Protein Precursor (metabolism)</term><term>Apolipoprotein E4 (metabolism)</term><term>Cerebellar Cortex (metabolism)</term><term>Essential Tremor (metabolism)</term><term>Female</term><term>Humans</term><term>Male</term><term>Membrane Proteins (metabolism)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neurofilament Proteins (metabolism)</term><term>Parietal Lobe (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Peptide Fragments (metabolism)</term><term>Phosphorylation</term><term>Purkinje Cells (metabolism)</term><term>Temporal Lobe (metabolism)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Amyloid beta-Protein Precursor</term><term>Apolipoprotein E4</term><term>Membrane Proteins</term><term>Nerve Tissue Proteins</term><term>Neurofilament Proteins</term><term>Peptide Fragments</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Cerebellar Cortex</term><term>Essential Tremor</term><term>Parietal Lobe</term><term>Parkinson Disease</term><term>Purkinje Cells</term><term>Temporal Lobe</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Phosphorylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The accumulation of insoluble amyloid-beta (Aβ) peptides is associated with neurodegenerative disorders, such as Alzheimer's disease (AD). As essential tremor (ET) could involve neurodegenerative processes in the cerebellum, we quantified soluble and insoluble Aβ in cerebellar cortices from patients diagnosed with ET (n=9), compared to Controls (n=16) or individuals with Parkinson's disease (n=10). Although ante-mortem cognitive performance was not documented, all individuals included had the diagnosis of AD ruled out by a neuropathologist. ELISA-determined concentrations of insoluble Aβ42 in ET patients displayed a bimodal distribution, with a median 246-fold higher than in Controls (P<0.01, Kruskal-Wallis). Higher Aβ42 concentrations were measured in the parietal cortex of the same ET patients, compared to Controls (107-fold median increase, P<0.01, Kruskal-Wallis), but similar phosphorylated tau levels were detected. The rise in cerebellar insoluble Aβ42 concentrations is not associated to APP expression and processing or the ApoE4 status. However, Aβ42 levels in ET individuals were correlated with cerebellar insoluble phosphorylated tau (r(2)=0.71, P=0.005), unphosphorylated neurofilament heavy chain (NF-H; r(2)=0.50, P=0.030) and Lingo-1 (r(2)=0.73, P=0.007), indicative of a generalized neurodegenerative process involving the cerebellum. Our results suggest prevalent accumulations of insoluble Aβ42 in the cerebellum of ET, but not in age-matched PD. Whether this anomaly plays a role in ET symptoms warrants further investigations.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26253607</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>09</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>82</Volume><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Accumulation of amyloid-β in the cerebellar cortex of essential tremor patients.</ArticleTitle><Pagination><MedlinePgn>397-408</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2015.07.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(15)30020-6</ELocationID><Abstract><AbstractText>The accumulation of insoluble amyloid-beta (Aβ) peptides is associated with neurodegenerative disorders, such as Alzheimer's disease (AD). As essential tremor (ET) could involve neurodegenerative processes in the cerebellum, we quantified soluble and insoluble Aβ in cerebellar cortices from patients diagnosed with ET (n=9), compared to Controls (n=16) or individuals with Parkinson's disease (n=10). Although ante-mortem cognitive performance was not documented, all individuals included had the diagnosis of AD ruled out by a neuropathologist. ELISA-determined concentrations of insoluble Aβ42 in ET patients displayed a bimodal distribution, with a median 246-fold higher than in Controls (P<0.01, Kruskal-Wallis). Higher Aβ42 concentrations were measured in the parietal cortex of the same ET patients, compared to Controls (107-fold median increase, P<0.01, Kruskal-Wallis), but similar phosphorylated tau levels were detected. The rise in cerebellar insoluble Aβ42 concentrations is not associated to APP expression and processing or the ApoE4 status. However, Aβ42 levels in ET individuals were correlated with cerebellar insoluble phosphorylated tau (r(2)=0.71, P=0.005), unphosphorylated neurofilament heavy chain (NF-H; r(2)=0.50, P=0.030) and Lingo-1 (r(2)=0.73, P=0.007), indicative of a generalized neurodegenerative process involving the cerebellum. Our results suggest prevalent accumulations of insoluble Aβ42 in the cerebellum of ET, but not in age-matched PD. Whether this anomaly plays a role in ET symptoms warrants further investigations.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Béliveau</LastName><ForeName>Eric</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tremblay</LastName><ForeName>Cyntia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Aubry-Lafontaine</LastName><ForeName>Émilie</ForeName><Initials>É</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paris-Robidas</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delay</LastName><ForeName>Charlotte</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robinson</LastName><ForeName>Chris</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferguson</LastName><ForeName>Les</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>Ali H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>Alex</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, SK, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Calon</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Faculty of Pharmacy, Université Laval, Québec, QC, Canada; Neurosciences Axis, Centre de recherche du CHU de Québec, Québec, QC, Canada. Electronic address: frederic.calon@crchul.ulaval.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C545487">APP protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016564">Amyloid beta-Protein Precursor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053327">Apolipoprotein E4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C482293">LINGO1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C054369">MAPT protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016900">Neurofilament Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010446">Peptide Fragments</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C078592">amyloid beta-protein (1-40)</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C075222">amyloid beta-protein (1-42)</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>108688-71-7</RegistryNumber><NameOfSubstance UI="C051774">neurofilament protein H</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016229" MajorTopicYN="N">Amyloid beta-Peptides</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016564" MajorTopicYN="N">Amyloid beta-Protein Precursor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053327" MajorTopicYN="N">Apolipoprotein E4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002525" MajorTopicYN="N">Cerebellar Cortex</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020329" MajorTopicYN="N">Essential Tremor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009419" MajorTopicYN="N">Nerve Tissue Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016900" MajorTopicYN="N">Neurofilament Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010296" MajorTopicYN="N">Parietal Lobe</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010446" MajorTopicYN="N">Peptide Fragments</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011689" MajorTopicYN="N">Purkinje Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013702" MajorTopicYN="N">Temporal Lobe</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Amyloid beta</Keyword><Keyword MajorTopicYN="N">Cerebellum</Keyword><Keyword MajorTopicYN="N">Essential tremor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>03</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>07</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>8</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>8</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>8</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26253607</ArticleId><ArticleId IdType="pii">S0969-9961(15)30020-6</ArticleId><ArticleId IdType="doi">10.1016/j.nbd.2015.07.016</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Beliveau, Eric" sort="Beliveau, Eric" uniqKey="Beliveau E" first="Eric" last="Béliveau">Eric Béliveau</name></noRegion><name sortKey="Aubry Lafontaine, Emilie" sort="Aubry Lafontaine, Emilie" uniqKey="Aubry Lafontaine E" first="Émilie" last="Aubry-Lafontaine">Émilie Aubry-Lafontaine</name><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><name sortKey="Delay, Charlotte" sort="Delay, Charlotte" uniqKey="Delay C" first="Charlotte" last="Delay">Charlotte Delay</name><name sortKey="Ferguson, Les" sort="Ferguson, Les" uniqKey="Ferguson L" first="Les" last="Ferguson">Les Ferguson</name><name sortKey="Paris Robidas, Sarah" sort="Paris Robidas, Sarah" uniqKey="Paris Robidas S" first="Sarah" last="Paris-Robidas">Sarah Paris-Robidas</name><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H" last="Rajput">Ali H. Rajput</name><name sortKey="Robinson, Chris" sort="Robinson, Chris" uniqKey="Robinson C" first="Chris" last="Robinson">Chris Robinson</name><name sortKey="Tremblay, Cyntia" sort="Tremblay, Cyntia" uniqKey="Tremblay C" first="Cyntia" last="Tremblay">Cyntia Tremblay</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Accumulation of amyloid-β in the cerebellar cortex of essential tremor patients.
}}
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