Cerebrospinal fluid biomarkers for assessing Huntington disease onset and severity
NRC publication: Yes
Saved in:
Published in | Brain communications Vol. 4; no. 6; p. fcac309 |
---|---|
Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
2022
|
Subjects | |
Online Access | Get full text |
ISSN | 2632-1297 2632-1297 |
DOI | 10.1093/braincomms/fcac309 |
Cover
Abstract | NRC publication: Yes The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings. |
---|---|
AbstractList | The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings. The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings. Caron et al. report novel multi-marker CSF protein combinations that accurately discriminate between individuals based on Huntington’s disease mutation status and disease severity. These exploratory CSF biomarker panels may improve the accuracy of disease-onset predictions and complement clinical and imaging biomarkers for monitoring disease severity and therapeutic response. Graphical abstract The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings.The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings. NRC publication: Yes |
Author | Aly, Amirah E Caron, Nicholas S Sandhu, Akshdeep Abulrob, Abedelnasser Hayden, Michael R Findlay Black, Hailey Leavitt, Blair R Bone, Jeffrey N Stanimirovic, Danica Haqqani, Arsalan S McBride, Jodi L |
Author_xml | – sequence: 1 fullname: Caron, Nicholas S – sequence: 2 fullname: Haqqani, Arsalan S – sequence: 3 fullname: Sandhu, Akshdeep – sequence: 4 fullname: Aly, Amirah E – sequence: 5 fullname: Findlay Black, Hailey – sequence: 6 fullname: Bone, Jeffrey N – sequence: 7 fullname: McBride, Jodi L – sequence: 8 fullname: Abulrob, Abedelnasser – sequence: 9 fullname: Stanimirovic, Danica – sequence: 10 fullname: Leavitt, Blair R – sequence: 11 fullname: Hayden, Michael R |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36523269$$D View this record in MEDLINE/PubMed |
BookMark | eNp9UctuFDEQtFAQCSE_wAHNkcsSjx8z4wsSWgWCFCkSgrPVttvBMGsvtidS_h4vu-TBgYvLj6rqdtdLchRTREJe9_RdTxU_NxlCtGmzKefeguVUPSMnbOBs1TM1Hj3aH5OzUn5QSpkUkqvpBTnmg2ScDeqEfFljRpNT2YYIc-fnJbjOhLSB_BNz6XzKHZSCpYR4010usTasKXYuFISCXYoFawfRdQVvMYd694o89zAXPDvgKfn28eLr-nJ1df3p8_rD1coKJesKEE0P1DBmhaWjs1b0OAnTS6ZQSj_aaaQD8kk4Lzg2DvcIRvqBW8Gp56fk_d53u5gNOouxZpj1NofW_J1OEPTTlxi-65t0q9UohkHRZvD2YJDTrwVL1ZtQLM4zRExL0WyUUo4jp6xR3zyudV_k7yAbge0Jts2yZPT3lJ7qXWD6ITB9CKyJpn9ENlSoIe36DfP_pW4vjdlaiODgycdtKDXosAPdGNr-WWB_H7fQTnJiqBC8ZlM_asEmqoEqpznzRnjmhDKU_wZOvceq |
CitedBy_id | crossref_primary_10_3390_pharmaceutics15112549 crossref_primary_10_1093_braincomms_fcae030 crossref_primary_10_3390_biology12121500 crossref_primary_10_1038_s41591_024_03424_6 crossref_primary_10_1080_13543784_2024_2348738 crossref_primary_10_1016_j_neuri_2024_100176 crossref_primary_10_3390_brainsci15010076 crossref_primary_10_3390_metabo13121203 crossref_primary_10_1042_CS20230513 crossref_primary_10_3390_biomedicines11082275 crossref_primary_10_3390_ijms25084323 crossref_primary_10_3390_biology14020129 crossref_primary_10_1016_j_xcrm_2023_101314 crossref_primary_10_1186_s40035_024_00443_8 crossref_primary_10_3390_jpm14040380 crossref_primary_10_54393_pjhs_v5i09_2153 |
Cites_doi | 10.1081/RRS-200029981 10.1126/scitranslmed.aat7108 10.1212/WNL.0000000000004743 10.1111/ene.12750 10.1002/ana.410410521 10.1016/j.jchemneu.2004.02.005 10.1007/s00401-020-02183-1 10.1186/1750-1326-6-37 10.3233/JAD-150351 10.1073/pnas.1204366109 10.1371/journal.pone.0163479 10.1038/srep45477 10.1093/nar/gkz369 10.1007/s00415-010-5876-x 10.1016/0092-8674(93)90585-E 10.1111/j.1399-0004.2004.00241.x 10.1093/hmg/9.9.1259 10.1002/mds.28391 10.1111/jnc.12350 10.1523/JNEUROSCI.4248-11.2012 10.1016/S1474-4422(13)70088-7 10.1021/acs.analchem.1c03782 10.1056/NEJMoa1900907 10.3233/JHD-170273 10.1038/nature09667 10.1126/science.1059581 10.1016/0304-3940(91)90583-F 10.1093/hmg/ddp527 10.1016/j.cell.2015.07.003 10.1523/JNEUROSCI.0676-04.2004 10.1074/mcp.RA117.000023 10.1038/srep41316 10.1212/NXI.0000000000000287 10.1074/mcp.M800231-MCP200 10.1021/pr0700753 10.1016/S0306-4522(00)00008-7 10.1371/journal.pone.0233820 10.1038/s41598-021-83000-x 10.1016/S1474-4422(11)70263-0 10.1038/s41598-019-45237-5 10.3389/fnins.2021.689938 10.1523/JNEUROSCI.0111-12.2012 10.1016/j.nbd.2011.03.006 10.1073/pnas.0308679101 10.1126/scitranslmed.abc2888 10.1007/978-1-59745-188-8_17 10.1371/journal.pcbi.1005752 10.1212/WNL.0000000000005005 10.3389/fimmu.2019.00362 10.3233/JHD-160196 10.1039/C9AN01893J 10.1038/srep12166 10.1016/j.nbd.2016.10.006 10.1021/mp3004995 10.1172/JCI80743 10.1006/exnr.1999.7170 10.3233/JHD-170269 10.1016/j.ajhg.2019.04.007 10.1007/BF02257671 10.1016/S0006-8993(00)02237-X 10.2307/2531595 10.1016/j.parkreldis.2008.05.012 10.1002/mds.870110204 10.1007/BF00310376 10.1002/ana.410270217 10.1021/acs.analchem.9b05685 10.1002/mds.28300 10.1371/journal.pone.0193492 10.1371/journal.pone.0015809 10.1038/nrneurol.2014.24 10.1016/j.parkreldis.2021.04.017 10.1002/ana.24406 10.1016/S1474-4422(17)30124-2 10.1016/j.expneurol.2013.08.019 10.1038/ng0893-398 10.1016/j.cell.2019.06.036 10.1093/hmg/ddl013 10.1073/pnas.85.15.5733 |
ContentType | Journal Article |
Copyright | Creative Commons, Attribution 4.0 International (CC BY 4.0) (https://creativecommons.org/licenses/by/4.0/) Creative Commons, Attribution 4.0 International (CC BY 4.0) (https://creativecommons.org/licenses/by/4.0/deed.fr) The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. 2022 |
Copyright_xml | – notice: Creative Commons, Attribution 4.0 International (CC BY 4.0) (https://creativecommons.org/licenses/by/4.0/) Creative Commons, Attribution 4.0 International (CC BY 4.0) (https://creativecommons.org/licenses/by/4.0/deed.fr) – notice: The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. – notice: The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. 2022 |
DBID | -LJ GXV AAYXX CITATION NPM 7X8 5PM |
DOI | 10.1093/braincomms/fcac309 |
DatabaseName | National Research Council Canada Archive CISTI Source CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef PubMed MEDLINE - Academic |
DatabaseTitleList | CrossRef MEDLINE - Academic PubMed |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Sciences |
EISSN | 2632-1297 |
ExternalDocumentID | PMC9746690 36523269 10_1093_braincomms_fcac309 oai_cisti_icist_nrc_cnrc_ca_cistinparc_582e9eaf_2817_4280_a09d_32fb4f2d49b0 |
Genre | Journal Article |
GrantInformation_xml | – fundername: ; – fundername: ; grantid: F17-01276 – fundername: ; grantid: F17–00391 |
GroupedDBID | -LJ 0R~ 53G AAFWJ AAPXW AAVAP ABEJV ABGNP ABPTD ABXVV AFPKN ALMA_UNASSIGNED_HOLDINGS AMNDL EBS EMOBN GROUPED_DOAJ GXV KSI M~E OK1 RPM TOX AAYXX CITATION AFULF NPM ROX 7X8 5PM |
ID | FETCH-LOGICAL-c495t-aeeb1a0b22c4c07dcc41e84b1529e55f7c8706e384df43e4c03feab5f63c430f3 |
ISSN | 2632-1297 |
IngestDate | Tue Sep 30 17:17:41 EDT 2025 Fri Jul 11 04:14:54 EDT 2025 Wed Feb 19 02:26:15 EST 2025 Thu Apr 24 22:55:46 EDT 2025 Tue Jul 01 04:46:20 EDT 2025 Fri Sep 26 16:37:55 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 6 |
Keywords | proenkephalin neurofilament light biomarkers CSF Huntington disease |
Language | English |
License | https://creativecommons.org/licenses/by/4.0 The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c495t-aeeb1a0b22c4c07dcc41e84b1529e55f7c8706e384df43e4c03feab5f63c430f3 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ORCID | 0000-0001-5194-7892 0000-0002-3877-455X |
OpenAccessLink | http://dx.doi.org/10.1093/braincomms/fcac309 |
PMID | 36523269 |
PQID | 2755577302 |
PQPubID | 23479 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_9746690 proquest_miscellaneous_2755577302 pubmed_primary_36523269 crossref_primary_10_1093_braincomms_fcac309 crossref_citationtrail_10_1093_braincomms_fcac309 nrccanada_primary_oai_cisti_icist_nrc_cnrc_ca_cistinparc_582e9eaf_2817_4280_a09d_32fb4f2d49b0 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2022-00-00 |
PublicationDateYYYYMMDD | 2022-01-01 |
PublicationDate_xml | – year: 2022 text: 2022-00-00 |
PublicationDecade | 2020 |
PublicationPlace | England |
PublicationPlace_xml | – name: England – name: US |
PublicationTitle | Brain communications |
PublicationTitleAlternate | Brain Commun |
PublicationYear | 2022 |
Publisher | Oxford University Press |
Publisher_xml | – name: Oxford University Press |
References | Hedreen (2022121316304672100_fcac309-B6) 1991; 133 Heinsen (2022121316304672100_fcac309-B7) 1994; 88 Andrew (2022121316304672100_fcac309-B9) 1993; 4 Cifani (2022121316304672100_fcac309-B35) 2017; 16 Chen (2022121316304672100_fcac309-B71) 2011; 469 Nguyen (2022121316304672100_fcac309-B37) 2019; 9 Huntington Study Group (2022121316304672100_fcac309-B16) 1996; 11 Wild (2022121316304672100_fcac309-B23) 2015; 125 Penney (2022121316304672100_fcac309-B51) 1997; 41 Di Pardo (2022121316304672100_fcac309-B69) 2017; 7 Huang (2022121316304672100_fcac309-B66) 2011; 6 Tabrizi (2022121316304672100_fcac309-B18) 2012; 11 Wexler (2022121316304672100_fcac309-B15) 2004; 101 Yu (2022121316304672100_fcac309-B80) 2020; 92 Raudvere (2022121316304672100_fcac309-B59) 2019; 47 Carpanini (2022121316304672100_fcac309-B77) 2019; 10 Tham (2022121316304672100_fcac309-B75) 1993; 5 Reiner (2022121316304672100_fcac309-B3) 1988; 85 Glass (2022121316304672100_fcac309-B4) 2000; 97 Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium (2022121316304672100_fcac309-B12) 2015; 162 Drouin-Ouellet (2022121316304672100_fcac309-B68) 2015; 78 Fang (2022121316304672100_fcac309-B38) 2009; 8 Niemela (2022121316304672100_fcac309-B41) 2021; 36 Ou (2022121316304672100_fcac309-B63) 2021; 11 Vinther-Jensen (2022121316304672100_fcac309-B30) 2016; 3 Zuccato (2022121316304672100_fcac309-B64) 2001; 293 Mazarei (2022121316304672100_fcac309-B48) 2010; 19 Haqqani (2022121316304672100_fcac309-B53) 2008; 439 Johnson (2022121316304672100_fcac309-B29) 2018; 90 Southwell (2022121316304672100_fcac309-B22) 2015; 5 Cudkowicz (2022121316304672100_fcac309-B5) 1990; 27 Mievis (2022121316304672100_fcac309-B76) 2011; 42 Brzhozovskiy (2022121316304672100_fcac309-B36) 2022; 94 Wright (2022121316304672100_fcac309-B14) 2019; 104 Rodrigues (2022121316304672100_fcac309-B25) 2020; 12 Bracko (2022121316304672100_fcac309-B73) 2012; 32 Ferrer (2022121316304672100_fcac309-B62) 2000; 866 Tabrizi (2022121316304672100_fcac309-B19) 2013; 12 Deng (2022121316304672100_fcac309-B2) 2004; 27 Dalrymple (2022121316304672100_fcac309-B40) 2007; 6 Niemela (2022121316304672100_fcac309-B32) 2018; 13 Schobel (2022121316304672100_fcac309-B17) 2017; 89 Hodges (2022121316304672100_fcac309-B44) 2006; 15 Byrne (2022121316304672100_fcac309-B20) 2016; 5 Gaither (2022121316304672100_fcac309-B81) 2020; 145 Ross (2022121316304672100_fcac309-B8) 2014; 10 Ryskamp (2022121316304672100_fcac309-B46) 2017; 97 Luthi-Carter (2022121316304672100_fcac309-B47) 2000; 9 Singhrao (2022121316304672100_fcac309-B78) 1999; 159 Corvol (2022121316304672100_fcac309-B45) 2004; 24 DeLong (2022121316304672100_fcac309-B57) 1988; 44 Rohart (2022121316304672100_fcac309-B56) 2017; 13 Shi (2022121316304672100_fcac309-B79) 2012; 109 Byrne (2022121316304672100_fcac309-B27) 2017; 16 Byrne (2022121316304672100_fcac309-B24) 2018; 10 Yuan (2022121316304672100_fcac309-B34) 2021; 15 Mazarei (2022121316304672100_fcac309-B49) 2013; 127 Schmeisser (2022121316304672100_fcac309-B72) 2012; 32 Silajdzic (2022121316304672100_fcac309-B21) 2018; 7 Al Shweiki (2022121316304672100_fcac309-B42) 2021; 36 Tabrizi (2022121316304672100_fcac309-B33) 2019; 380 Genetic Modifiers of Huntington’s Disease Consortium. Electronic address ghmhe, Genetic Modifiers of Huntington’s Disease (GeM-HD) Consortium (2022121316304672100_fcac309-B13) 2019; 178 Rodrigues (2022121316304672100_fcac309-B39) 2016; 11 Jesse (2022121316304672100_fcac309-B65) 2011; 258 Kuhn (2022121316304672100_fcac309-B55) Mazzara (2022121316304672100_fcac309-B58) 2017; 7 The Huntington’s Disease Collaborative Research Group (2022121316304672100_fcac309-B1) 1993; 72 (2022121316304672100_fcac309-B54) 2020 Lowe (2022121316304672100_fcac309-B61) 2020; 15 Garcia-Huerta (2022121316304672100_fcac309-B50) 2020; 140 Langbehn (2022121316304672100_fcac309-B10) 2004; 65 Constantinescu (2022121316304672100_fcac309-B28) 2009; 15 Fodale (2022121316304672100_fcac309-B26) 2017; 6 Liang (2022121316304672100_fcac309-B60) 2011; 6 Parkin (2022121316304672100_fcac309-B31) 2021; 87 Neve (2022121316304672100_fcac309-B70) 2004; 24 Brinkman (2022121316304672100_fcac309-B11) 1997; 60 Haqqani (2022121316304672100_fcac309-B52) 2013; 10 Vinther-Jensen (2022121316304672100_fcac309-B43) 2015; 22 Lin (2022121316304672100_fcac309-B67) 2013; 250 Aberg (2022121316304672100_fcac309-B74) 2015; 48 |
References_xml | – volume: 24 start-page: 165 issue: 3 year: 2004 ident: 2022121316304672100_fcac309-B70 article-title: Dopamine receptor signaling publication-title: J Recept Signal Transduct Res doi: 10.1081/RRS-200029981 – volume: 10 issue: 458 year: 2018 ident: 2022121316304672100_fcac309-B24 article-title: Evaluation of mutant huntingtin and neurofilament proteins as potential markers in Huntington’s disease publication-title: Sci Transl Med doi: 10.1126/scitranslmed.aat7108 – volume: 89 start-page: 2495 issue: 24 year: 2017 ident: 2022121316304672100_fcac309-B17 article-title: Motor, cognitive, and functional declines contribute to a single progressive factor in early HD publication-title: Neurology doi: 10.1212/WNL.0000000000004743 – volume: 22 start-page: 1378 issue: 10 year: 2015 ident: 2022121316304672100_fcac309-B43 article-title: Ubiquitin: A potential cerebrospinal fluid progression marker in Huntington’s disease publication-title: Eur J Neurol doi: 10.1111/ene.12750 – volume: 41 start-page: 689 issue: 5 year: 1997 ident: 2022121316304672100_fcac309-B51 article-title: CAG Repeat number governs the development rate of pathology in Huntington’s disease publication-title: Ann Neurol doi: 10.1002/ana.410410521 – volume: 27 start-page: 143 issue: 3 year: 2004 ident: 2022121316304672100_fcac309-B2 article-title: Differential loss of striatal projection systems in Huntington’s disease: A quantitative immunohistochemical study publication-title: J Chem Neuroanat doi: 10.1016/j.jchemneu.2004.02.005 – volume: 140 start-page: 737 issue: 5 year: 2020 ident: 2022121316304672100_fcac309-B50 article-title: Insulin-like growth factor 2 (IGF2) protects against Huntington’s disease through the extracellular disposal of protein aggregates publication-title: Acta Neuropathol doi: 10.1007/s00401-020-02183-1 – volume: 6 start-page: 37 year: 2011 ident: 2022121316304672100_fcac309-B60 article-title: Reduction of mutant huntingtin accumulation and toxicity by lysosomal cathepsins D and B in neurons publication-title: Mol Neurodegener doi: 10.1186/1750-1326-6-37 – volume: 48 start-page: 637 issue: 3 year: 2015 ident: 2022121316304672100_fcac309-B74 article-title: Increased cerebrospinal fluid level of insulin-like growth factor-II in male patients with Alzheimer’s disease publication-title: J Alzheimers Dis doi: 10.3233/JAD-150351 – volume: 109 start-page: 15395 issue: 38 year: 2012 ident: 2022121316304672100_fcac309-B79 article-title: Antibody-free, targeted mass-spectrometric approach for quantification of proteins at low picogram per milliliter levels in human plasma/serum publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1204366109 – volume: 11 start-page: e0163479 issue: 9 year: 2016 ident: 2022121316304672100_fcac309-B39 article-title: Cerebrospinal fluid inflammatory biomarkers reflect clinical severity in Huntington’s disease publication-title: PLoS One doi: 10.1371/journal.pone.0163479 – volume: 7 start-page: 45477 year: 2017 ident: 2022121316304672100_fcac309-B58 article-title: CombiROC: An interactive web tool for selecting accurate marker combinations of omics data publication-title: Sci Rep doi: 10.1038/srep45477 – volume: 47 start-page: W191 issue: W1 year: 2019 ident: 2022121316304672100_fcac309-B59 article-title: G:Profiler: A web server for functional enrichment analysis and conversions of gene lists (2019 update) publication-title: Nucleic Acids Res doi: 10.1093/nar/gkz369 – volume: 258 start-page: 1034 issue: 6 year: 2011 ident: 2022121316304672100_fcac309-B65 article-title: Summary of cerebrospinal fluid routine parameters in neurodegenerative diseases publication-title: J Neurol doi: 10.1007/s00415-010-5876-x – volume: 72 start-page: 971 issue: 6 year: 1993 ident: 2022121316304672100_fcac309-B1 article-title: A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes publication-title: Cell doi: 10.1016/0092-8674(93)90585-E – volume: 65 start-page: 267 issue: 4 year: 2004 ident: 2022121316304672100_fcac309-B10 article-title: A new model for prediction of the age of onset and penetrance for Huntington’s disease based on CAG length publication-title: Clin Genet doi: 10.1111/j.1399-0004.2004.00241.x – volume: 9 start-page: 1259 issue: 9 year: 2000 ident: 2022121316304672100_fcac309-B47 article-title: Decreased expression of striatal signaling genes in a mouse model of Huntington’s disease publication-title: Hum Mol Genet doi: 10.1093/hmg/9.9.1259 – volume: 36 start-page: 481 issue: 2 year: 2021 ident: 2022121316304672100_fcac309-B41 article-title: Proenkephalin decreases in cerebrospinal fluid with symptom progression of Huntington’s disease publication-title: Mov Disord doi: 10.1002/mds.28391 – volume: 127 start-page: 852 issue: 6 year: 2013 ident: 2022121316304672100_fcac309-B49 article-title: Age-dependent alterations of the kynurenine pathway in the YAC128 mouse model of Huntington disease publication-title: J Neurochem doi: 10.1111/jnc.12350 – volume: 32 start-page: 3376 issue: 10 year: 2012 ident: 2022121316304672100_fcac309-B73 article-title: Gene expression profiling of neural stem cells and their neuronal progeny reveals IGF2 as a regulator of adult hippocampal neurogenesis publication-title: J Neurosci doi: 10.1523/JNEUROSCI.4248-11.2012 – volume: 12 start-page: 637 issue: 7 year: 2013 ident: 2022121316304672100_fcac309-B19 article-title: Predictors of phenotypic progression and disease onset in premanifest and early-stage Huntington’s disease in the TRACK-HD study: Analysis of 36-month observational data publication-title: Lancet Neurol doi: 10.1016/S1474-4422(13)70088-7 – volume: 94 start-page: 2016 issue: 4 year: 2022 ident: 2022121316304672100_fcac309-B36 article-title: The parallel reaction monitoring-parallel accumulation-serial fragmentation (prm-PASEF) approach for multiplexed absolute quantitation of proteins in human plasma publication-title: Anal Chem doi: 10.1021/acs.analchem.1c03782 – volume: 380 start-page: 2307 issue: 24 year: 2019 ident: 2022121316304672100_fcac309-B33 article-title: Targeting huntingtin expression in patients with Huntington’s disease publication-title: N Engl J Med doi: 10.1056/NEJMoa1900907 – volume: 7 start-page: 109 issue: 2 year: 2018 ident: 2022121316304672100_fcac309-B21 article-title: A critical evaluation of wet biomarkers for Huntington’s disease: Current Status and ways forward publication-title: J Huntingtons Dis doi: 10.3233/JHD-170273 – volume: 469 start-page: 491 issue: 7331 year: 2011 ident: 2022121316304672100_fcac309-B71 article-title: A critical role for IGF-II in memory consolidation and enhancement publication-title: Nature doi: 10.1038/nature09667 – volume: 293 start-page: 493 issue: 5529 year: 2001 ident: 2022121316304672100_fcac309-B64 article-title: Loss of huntingtin-mediated BDNF gene transcription in Huntington’s disease publication-title: Science doi: 10.1126/science.1059581 – volume: 133 start-page: 257 issue: 2 year: 1991 ident: 2022121316304672100_fcac309-B6 article-title: Neuronal loss in layers V and VI of cerebral cortex in Huntington’s disease publication-title: Neurosci Lett doi: 10.1016/0304-3940(91)90583-F – volume: 19 start-page: 609 issue: 4 year: 2010 ident: 2022121316304672100_fcac309-B48 article-title: Expression analysis of novel striatal-enriched genes in Huntington disease publication-title: Hum Mol Genet doi: 10.1093/hmg/ddp527 – volume: 162 start-page: 516 issue: 3 year: 2015 ident: 2022121316304672100_fcac309-B12 article-title: Identification of genetic factors that modify clinical onset of Huntington’s disease publication-title: Cell doi: 10.1016/j.cell.2015.07.003 – volume: 24 start-page: 7007 issue: 31 year: 2004 ident: 2022121316304672100_fcac309-B45 article-title: Persistent increase in olfactory type G-protein alpha subunit levels may underlie D1 receptor functional hypersensitivity in Parkinson disease publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0676-04.2004 – volume: 16 start-page: 2006 issue: 11 year: 2017 ident: 2022121316304672100_fcac309-B35 article-title: High sensitivity quantitative proteomics using automated multidimensional nano-flow chromatography and accumulated ion monitoring on quadrupole-orbitrap-linear ion trap mass spectrometer publication-title: Mol Cell Proteomics doi: 10.1074/mcp.RA117.000023 – volume: 7 start-page: 41316 year: 2017 ident: 2022121316304672100_fcac309-B69 article-title: Impairment of blood-brain barrier is an early event in R6/2 mouse model of Huntington disease publication-title: Sci Rep doi: 10.1038/srep41316 – volume: 3 start-page: e287 issue: 6 year: 2016 ident: 2022121316304672100_fcac309-B30 article-title: Selected CSF biomarkers indicate no evidence of early neuroinflammation in Huntington disease publication-title: Neurol Neuroimmunol Neuroinflamm doi: 10.1212/NXI.0000000000000287 – volume: 8 start-page: 451 issue: 3 year: 2009 ident: 2022121316304672100_fcac309-B38 article-title: Brain-specific proteins decline in the cerebrospinal fluid of humans with Huntington disease publication-title: Mol Cell Proteomics doi: 10.1074/mcp.M800231-MCP200 – volume: 6 start-page: 2833 issue: 7 year: 2007 ident: 2022121316304672100_fcac309-B40 article-title: Proteomic profiling of plasma in Huntington’s disease reveals neuroinflammatory activation and biomarker candidates publication-title: J Proteome Res doi: 10.1021/pr0700753 – volume: 97 start-page: 505 issue: 3 year: 2000 ident: 2022121316304672100_fcac309-B4 article-title: The pattern of neurodegeneration in Huntington’s disease: A comparative study of cannabinoid, dopamine, adenosine and GABA(A) receptor alterations in the human basal ganglia in Huntington’s disease publication-title: Neuroscience doi: 10.1016/S0306-4522(00)00008-7 – volume: 15 start-page: e0233820 issue: 8 year: 2020 ident: 2022121316304672100_fcac309-B61 article-title: Cerebrospinal fluid endo-lysosomal proteins as potential biomarkers for Huntington’s disease publication-title: PLoS One doi: 10.1371/journal.pone.0233820 – volume: 11 start-page: 3481 issue: 1 year: 2021 ident: 2022121316304672100_fcac309-B63 article-title: Brain-derived neurotrophic factor in cerebrospinal fluid and plasma is not a biomarker for Huntington’s disease publication-title: Sci Rep doi: 10.1038/s41598-021-83000-x – volume: 11 start-page: 42 issue: 1 year: 2012 ident: 2022121316304672100_fcac309-B18 article-title: Potential endpoints for clinical trials in premanifest and early Huntington’s disease in the TRACK-HD study: Analysis of 24 month observational data publication-title: Lancet Neurol doi: 10.1016/S1474-4422(11)70263-0 – volume: 9 start-page: 8836 issue: 1 year: 2019 ident: 2022121316304672100_fcac309-B37 article-title: A sensitive and simple targeted proteomics approach to quantify transcription factor and membrane proteins of the unfolded protein response pathway in glioblastoma cells publication-title: Sci Rep doi: 10.1038/s41598-019-45237-5 – volume: 15 start-page: 689938 year: 2021 ident: 2022121316304672100_fcac309-B34 article-title: Neurofilament proteins as biomarkers to monitor neurological diseases and the efficacy of therapies publication-title: Front Neurosci doi: 10.3389/fnins.2021.689938 – volume: 32 start-page: 5688 issue: 16 year: 2012 ident: 2022121316304672100_fcac309-B72 article-title: Ikappab kinase/nuclear factor kappaB-dependent insulin-like growth factor 2 (Igf2) expression regulates synapse formation and spine maturation via Igf2 receptor signaling publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0111-12.2012 – volume: 42 start-page: 524 issue: 3 year: 2011 ident: 2022121316304672100_fcac309-B76 article-title: Worsening of Huntington disease phenotype in CB1 receptor knockout mice publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2011.03.006 – volume: 101 start-page: 3498 issue: 10 year: 2004 ident: 2022121316304672100_fcac309-B15 article-title: Venezuelan kindreds reveal that genetic and environmental factors modulate Huntington’s disease age of onset publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.0308679101 – volume: 12 issue: 574 year: 2020 ident: 2022121316304672100_fcac309-B25 article-title: Mutant huntingtin and neurofilament light have distinct longitudinal dynamics in Huntington’s disease publication-title: Sci Transl Med doi: 10.1126/scitranslmed.abc2888 – volume: 439 start-page: 241 year: 2008 ident: 2022121316304672100_fcac309-B53 article-title: Quantitative protein profiling by mass spectrometry using label-free proteomics publication-title: Methods Mol Biol doi: 10.1007/978-1-59745-188-8_17 – volume: 13 start-page: e1005752 issue: 11 year: 2017 ident: 2022121316304672100_fcac309-B56 article-title: Mixomics: An R package for ‘omics feature selection and multiple data integration publication-title: PLoS Comput Biol doi: 10.1371/journal.pcbi.1005752 – volume: 90 start-page: e717 issue: 8 year: 2018 ident: 2022121316304672100_fcac309-B29 article-title: Neurofilament light protein in blood predicts regional atrophy in Huntington disease publication-title: Neurology doi: 10.1212/WNL.0000000000005005 – volume: 10 start-page: 362 year: 2019 ident: 2022121316304672100_fcac309-B77 article-title: Therapeutic inhibition of the complement system in diseases of the central nervous system publication-title: Front Immunol doi: 10.3389/fimmu.2019.00362 – volume: 5 start-page: 1 issue: 1 year: 2016 ident: 2022121316304672100_fcac309-B20 article-title: Cerebrospinal fluid biomarkers for Huntington’s disease publication-title: J Huntingtons Dis doi: 10.3233/JHD-160196 – volume: 145 start-page: 3634 issue: 10 year: 2020 ident: 2022121316304672100_fcac309-B81 article-title: Determination of the concentration range for 267 proteins from 21 lots of commercial human plasma using highly multiplexed multiple reaction monitoring mass spectrometry publication-title: Analyst doi: 10.1039/C9AN01893J – volume: 5 start-page: 12166 year: 2015 ident: 2022121316304672100_fcac309-B22 article-title: Ultrasensitive measurement of huntingtin protein in cerebrospinal fluid demonstrates increase with Huntington disease stage and decrease following brain huntingtin suppression publication-title: Sci Rep doi: 10.1038/srep12166 – volume: 97 start-page: 46 issue: Pt A year: 2017 ident: 2022121316304672100_fcac309-B46 article-title: The sigma-1 receptor mediates the beneficial effects of pridopidine in a mouse model of Huntington disease publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2016.10.006 – volume: 10 start-page: 1542 issue: 5 year: 2013 ident: 2022121316304672100_fcac309-B52 article-title: Multiplexed evaluation of serum and CSF pharmacokinetics of brain-targeting single-domain antibodies using a NanoLC-SRM-ILIS method publication-title: Mol Pharm doi: 10.1021/mp3004995 – ident: 2022121316304672100_fcac309-B55 – volume: 60 start-page: 1202 issue: 5 year: 1997 ident: 2022121316304672100_fcac309-B11 article-title: The likelihood of being affected with Huntington disease by a particular age, for a specific CAG size publication-title: Am J Hum Genet – volume: 125 start-page: 1979 issue: 5 year: 2015 ident: 2022121316304672100_fcac309-B23 article-title: Quantification of mutant huntingtin protein in cerebrospinal fluid from Huntington’s disease patients publication-title: J Clin Invest doi: 10.1172/JCI80743 – volume: 159 start-page: 362 issue: 2 year: 1999 ident: 2022121316304672100_fcac309-B78 article-title: Increased complement biosynthesis by microglia and complement activation on neurons in Huntington’s disease publication-title: Exp Neurol doi: 10.1006/exnr.1999.7170 – volume: 6 start-page: 349 issue: 4 year: 2017 ident: 2022121316304672100_fcac309-B26 article-title: Validation of ultrasensitive mutant huntingtin detection in human cerebrospinal fluid by single molecule counting immunoassay publication-title: J Huntingtons Dis doi: 10.3233/JHD-170269 – volume: 104 start-page: 1116 issue: 6 year: 2019 ident: 2022121316304672100_fcac309-B14 article-title: Length of uninterrupted CAG, independent of polyglutamine size, results in increased somatic instability, hastening onset of huntington disease publication-title: Am J Hum Genet doi: 10.1016/j.ajhg.2019.04.007 – volume: 5 start-page: 165 issue: 3 year: 1993 ident: 2022121316304672100_fcac309-B75 article-title: Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type publication-title: J Neural Transm Park Dis Dement Sect doi: 10.1007/BF02257671 – volume: 866 start-page: 257 issue: 1-2 year: 2000 ident: 2022121316304672100_fcac309-B62 article-title: Brain-derived neurotrophic factor in Huntington disease publication-title: Brain Res doi: 10.1016/S0006-8993(00)02237-X – volume-title: R: A language and environment for statistical computing year: 2020 ident: 2022121316304672100_fcac309-B54 – volume: 44 start-page: 837 issue: 3 year: 1988 ident: 2022121316304672100_fcac309-B57 article-title: Comparing the areas under two or more correlated receiver operating characteristic curves: A nonparametric approach publication-title: Biometrics doi: 10.2307/2531595 – volume: 15 start-page: 245 issue: 3 year: 2009 ident: 2022121316304672100_fcac309-B28 article-title: Levels of the light subunit of neurofilament triplet protein in cerebrospinal fluid in Huntington’s disease publication-title: Parkinsonism Relat Disord doi: 10.1016/j.parkreldis.2008.05.012 – volume: 11 start-page: 136 issue: 2 year: 1996 ident: 2022121316304672100_fcac309-B16 article-title: Unified Huntington’s disease rating scale: Reliability and consistency publication-title: Mov Disord doi: 10.1002/mds.870110204 – volume: 88 start-page: 320 issue: 4 year: 1994 ident: 2022121316304672100_fcac309-B7 article-title: Cortical and striatal neurone number in Huntington’s disease publication-title: Acta Neuropathol doi: 10.1007/BF00310376 – volume: 27 start-page: 200 issue: 2 year: 1990 ident: 2022121316304672100_fcac309-B5 article-title: Degeneration of pyramidal projection neurons in Huntington’s disease cortex publication-title: Ann Neurol doi: 10.1002/ana.410270217 – volume: 92 start-page: 6478 issue: 9 year: 2020 ident: 2022121316304672100_fcac309-B80 article-title: Benchmarking the orbitrap tribrid eclipse for next generation multiplexed proteomics publication-title: Anal Chem doi: 10.1021/acs.analchem.9b05685 – volume: 36 start-page: 492 issue: 2 year: 2021 ident: 2022121316304672100_fcac309-B42 article-title: Cerebrospinal fluid levels of prodynorphin-derived peptides are decreased in Huntington’s disease publication-title: Mov Disord doi: 10.1002/mds.28300 – volume: 13 start-page: e0193492 issue: 2 year: 2018 ident: 2022121316304672100_fcac309-B32 article-title: Cerebrospinal fluid sCD27 levels indicate active T cell-mediated inflammation in premanifest Huntington’s disease publication-title: PLoS One doi: 10.1371/journal.pone.0193492 – volume: 6 start-page: e15809 issue: 1 year: 2011 ident: 2022121316304672100_fcac309-B66 article-title: Increased prothrombin, apolipoprotein A-IV, and haptoglobin in the cerebrospinal fluid of patients with Huntington’s disease publication-title: PLoS One doi: 10.1371/journal.pone.0015809 – volume: 10 start-page: 204 issue: 4 year: 2014 ident: 2022121316304672100_fcac309-B8 article-title: Huntington disease: Natural history, biomarkers and prospects for therapeutics publication-title: Nat Rev Neurol doi: 10.1038/nrneurol.2014.24 – volume: 87 start-page: 32 year: 2021 ident: 2022121316304672100_fcac309-B31 article-title: Plasma neurofilament light in Huntington’s disease: A marker for disease onset, but not symptom progression publication-title: Parkinsonism Relat Disord doi: 10.1016/j.parkreldis.2021.04.017 – volume: 78 start-page: 160 issue: 2 year: 2015 ident: 2022121316304672100_fcac309-B68 article-title: Cerebrovascular and blood-brain barrier impairments in Huntington’s disease: Potential implications for its pathophysiology publication-title: Ann Neurol doi: 10.1002/ana.24406 – volume: 16 start-page: 601 issue: 8 year: 2017 ident: 2022121316304672100_fcac309-B27 article-title: Neurofilament light protein in blood as a potential biomarker of neurodegeneration in Huntington’s disease: A retrospective cohort analysis publication-title: Lancet Neurol doi: 10.1016/S1474-4422(17)30124-2 – volume: 250 start-page: 20 year: 2013 ident: 2022121316304672100_fcac309-B67 article-title: Neurovascular abnormalities in humans and mice with Huntington’s disease publication-title: Exp Neurol doi: 10.1016/j.expneurol.2013.08.019 – volume: 4 start-page: 398 issue: 4 year: 1993 ident: 2022121316304672100_fcac309-B9 article-title: The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington’s disease publication-title: Nat Genet doi: 10.1038/ng0893-398 – volume: 178 start-page: 887 issue: 4 year: 2019 ident: 2022121316304672100_fcac309-B13 article-title: CAG repeat not polyglutamine length determines timing of Huntington’s disease onset publication-title: Cell doi: 10.1016/j.cell.2019.06.036 – volume: 15 start-page: 965 issue: 6 year: 2006 ident: 2022121316304672100_fcac309-B44 article-title: Regional and cellular gene expression changes in human Huntington’s disease brain publication-title: Hum Mol Genet doi: 10.1093/hmg/ddl013 – volume: 85 start-page: 5733 issue: 15 year: 1988 ident: 2022121316304672100_fcac309-B3 article-title: Differential loss of striatal projection neurons in Huntington disease publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.85.15.5733 |
SSID | ssj0002545398 |
Score | 2.273808 |
Snippet | NRC publication: Yes The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define... |
SourceID | pubmedcentral proquest pubmed crossref nrccanada |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
StartPage | fcac309 |
SubjectTerms | biomarkers CSF Huntington disease neurofilament light Original proenkephalin |
Title | Cerebrospinal fluid biomarkers for assessing Huntington disease onset and severity |
URI | https://nrc-publications.canada.ca/eng/view/object/?id=582e9eaf-2817-4280-a09d-32fb4f2d49b0 https://www.ncbi.nlm.nih.gov/pubmed/36523269 https://www.proquest.com/docview/2755577302 https://pubmed.ncbi.nlm.nih.gov/PMC9746690 |
Volume | 4 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
journalDatabaseRights | – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 2632-1297 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002545398 issn: 2632-1297 databaseCode: DOA dateStart: 20190101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 2632-1297 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002545398 issn: 2632-1297 databaseCode: M~E dateStart: 20190101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre – providerCode: PRVAQN databaseName: PubMed Central customDbUrl: eissn: 2632-1297 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002545398 issn: 2632-1297 databaseCode: RPM dateStart: 20190101 isFulltext: true titleUrlDefault: https://www.ncbi.nlm.nih.gov/pmc/ providerName: National Library of Medicine – providerCode: PRVASL databaseName: Oxford Journals Open Access (Activated by CARLI) customDbUrl: eissn: 2632-1297 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0002545398 issn: 2632-1297 databaseCode: TOX dateStart: 20190701 isFulltext: true titleUrlDefault: https://academic.oup.com/journals/ providerName: Oxford University Press |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lj9MwELZgkYAL4k15rIKEuFRhEz-S5litdlWh3UWCVuoFWY5jqxW76SPthV_PTOwmDVRo4ZJGtls7ma-ep2cI-UBtkdmBVSHVSRbyVMdhDlpHqOLcZNQKFhV4dvjyKhlN-OepmLYe3fp0ySb_pH8ePFfyP1SFNqArnpL9B8o2PwoNcA_0hStQGK63ovGpWYNKi5U_UKa019s5iJPzxQ2G3KwrFyBZO3XRHjByRSEwjYb3yvQxktpFmAN_NFjGruPjxeoRGHPeniBpBHCMEyk9klA7rloT6kitVq5QVH-4rjBysu37BnPNtnXXj2pWGLNsAOcqXg9v5rD7-eMR3hhB9yyTmPc9BOHBcU9zoM1vt3wPVftbp9VKszpVwp_bukt5leNj41NXSJh2eDeL9tUXeT65uJDjs-n443IVYoExdMT7ait3yT2aglCyZ9hBpg16smB15eRm0f6IFcx90s584uftiDEPyrWuY_TUIT3l93DbPfll_Jg88opHMHQoekLumPIpuX_pQyueka8dMAU1mIIWTAGAKWjAFLRgCjyYghpMARA42IHpOZmcn41PR6EvuBFq0JM3oTLAuVWUU6q5jtJCax6bAc9BxsuMEDbV6BU3bMALy5mBMcwalQubMM1ZZNkLclQuSvOKBFGsRGRAOhJCcZborCgyBrcZTfK4iEWPxLv3J7XPRo9FUa6li4pgsn3n0r_zHuk331m6XCx_Hf29IUszHJOpa2Seco4fEkZIXV-Uay-XwF-kGFCTGWUlHcSpBA09kirKCsmozbmlBc_yqEfe70gtYUtGP5sqzWJbSZoKIVJgnbRHXjrSNwtgiQAdJoHVpR1QdFbY7SnnszrtO2j-SZJFr28x7xvyEP-dzlT4lhxt1lvzDoTnTX5cG52Oa_D_Akhx1Tg |
linkProvider | National Library of Medicine |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Cerebrospinal+fluid+biomarkers+for+assessing+Huntington+disease+onset+and+severity&rft.jtitle=Brain+communications&rft.au=Caron%2C+Nicholas+S&rft.au=Haqqani%2C+Arsalan+S&rft.au=Sandhu%2C+Akshdeep&rft.au=Aly%2C+Amirah+E&rft.date=2022&rft.issn=2632-1297&rft.eissn=2632-1297&rft.volume=4&rft.issue=6&rft.spage=fcac309&rft_id=info:doi/10.1093%2Fbraincomms%2Ffcac309&rft.externalDBID=NO_FULL_TEXT |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2632-1297&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2632-1297&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2632-1297&client=summon |