Plasma markers predict changes in amyloid, tau, atrophy and cognition in non-demented subjects

It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In this study, we sought to address this question by assessing whether plasma biomarkers can predict changes in amyloid load, tau accumulat...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Brain (London, England : 1878) Jg. 144; H. 9; S. 2826
Hauptverfasser:	Pereira, Joana B, Janelidze, Shorena, Stomrud, Erik, Palmqvist, Sebastian, van Westen, Danielle, Dage, Jeffrey L, Mattsson-Carlgren, Niklas, Hansson, Oskar
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England 22.10.2021
Schlagworte:	Adaptor Proteins, Signal Transducing - blood Adult Aged Aged, 80 and over Amyloid beta-Peptides - blood Atrophy - blood Biomarkers - blood Brain - diagnostic imaging Brain - metabolism Cohort Studies Female Humans Longitudinal Studies Male Middle Aged Neuropsychological Tests Peptide Fragments - blood Predictive Value of Tests amyloid-β plasma biomarkers cognition MRI PET tau PET
ISSN:	1460-2156, 1460-2156
Online-Zugang:	Weitere Angaben
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Abstract	It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In this study, we sought to address this question by assessing whether plasma biomarkers can predict changes in amyloid load, tau accumulation, brain atrophy and cognition in non-demented individuals. To achieve this, plasma amyloid-β 42/40 (Aβ42/40), phosphorylated-tau181, phosphorylated-tau217 and neurofilament light were determined in 159 non-demented individuals, 123 patients with Alzheimer's disease dementia and 35 patients with a non-Alzheimer's dementia from the Swedish BioFINDER-2 study, who underwent longitudinal amyloid (18F-flutemetamol) and tau (18F-RO948) PET, structural MRI (T1-weighted) and cognitive testing. Our univariate linear mixed effect models showed there were several significant associations between the plasma biomarkers with imaging and cognitive measures. However, when all biomarkers were included in the same multivariate linear mixed effect models, we found that increased longitudinal amyloid-PET signals were independently predicted by low baseline plasma Aβ42/40 (P = 0.012), whereas increased tau-PET signals, brain atrophy and worse cognition were independently predicted by high plasma phosphorylated-tau217 (P < 0.004). These biomarkers performed equally well or better than the corresponding biomarkers measured in the CSF. In addition, they showed a similar performance to binary plasma biomarker values defined using the Youden index, which can be more easily implemented in the clinic. In addition, plasma Aβ42/40 and phosphorylated-tau217 did not predict longitudinal changes in patients with a non-Alzheimer's neurodegenerative disorder. In conclusion, our findings indicate that plasma Aβ42/40 and phosphorylated-tau217 could be useful in clinical practice, research and drug development as prognostic markers of future Alzheimer's disease pathology.
AbstractList	It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In this study, we sought to address this question by assessing whether plasma biomarkers can predict changes in amyloid load, tau accumulation, brain atrophy and cognition in non-demented individuals. To achieve this, plasma amyloid-β 42/40 (Aβ42/40), phosphorylated-tau181, phosphorylated-tau217 and neurofilament light were determined in 159 non-demented individuals, 123 patients with Alzheimer's disease dementia and 35 patients with a non-Alzheimer's dementia from the Swedish BioFINDER-2 study, who underwent longitudinal amyloid (18F-flutemetamol) and tau (18F-RO948) PET, structural MRI (T1-weighted) and cognitive testing. Our univariate linear mixed effect models showed there were several significant associations between the plasma biomarkers with imaging and cognitive measures. However, when all biomarkers were included in the same multivariate linear mixed effect models, we found that increased longitudinal amyloid-PET signals were independently predicted by low baseline plasma Aβ42/40 (P = 0.012), whereas increased tau-PET signals, brain atrophy and worse cognition were independently predicted by high plasma phosphorylated-tau217 (P < 0.004). These biomarkers performed equally well or better than the corresponding biomarkers measured in the CSF. In addition, they showed a similar performance to binary plasma biomarker values defined using the Youden index, which can be more easily implemented in the clinic. In addition, plasma Aβ42/40 and phosphorylated-tau217 did not predict longitudinal changes in patients with a non-Alzheimer's neurodegenerative disorder. In conclusion, our findings indicate that plasma Aβ42/40 and phosphorylated-tau217 could be useful in clinical practice, research and drug development as prognostic markers of future Alzheimer's disease pathology.It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In this study, we sought to address this question by assessing whether plasma biomarkers can predict changes in amyloid load, tau accumulation, brain atrophy and cognition in non-demented individuals. To achieve this, plasma amyloid-β 42/40 (Aβ42/40), phosphorylated-tau181, phosphorylated-tau217 and neurofilament light were determined in 159 non-demented individuals, 123 patients with Alzheimer's disease dementia and 35 patients with a non-Alzheimer's dementia from the Swedish BioFINDER-2 study, who underwent longitudinal amyloid (18F-flutemetamol) and tau (18F-RO948) PET, structural MRI (T1-weighted) and cognitive testing. Our univariate linear mixed effect models showed there were several significant associations between the plasma biomarkers with imaging and cognitive measures. However, when all biomarkers were included in the same multivariate linear mixed effect models, we found that increased longitudinal amyloid-PET signals were independently predicted by low baseline plasma Aβ42/40 (P = 0.012), whereas increased tau-PET signals, brain atrophy and worse cognition were independently predicted by high plasma phosphorylated-tau217 (P < 0.004). These biomarkers performed equally well or better than the corresponding biomarkers measured in the CSF. In addition, they showed a similar performance to binary plasma biomarker values defined using the Youden index, which can be more easily implemented in the clinic. In addition, plasma Aβ42/40 and phosphorylated-tau217 did not predict longitudinal changes in patients with a non-Alzheimer's neurodegenerative disorder. In conclusion, our findings indicate that plasma Aβ42/40 and phosphorylated-tau217 could be useful in clinical practice, research and drug development as prognostic markers of future Alzheimer's disease pathology. It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In this study, we sought to address this question by assessing whether plasma biomarkers can predict changes in amyloid load, tau accumulation, brain atrophy and cognition in non-demented individuals. To achieve this, plasma amyloid-β 42/40 (Aβ42/40), phosphorylated-tau181, phosphorylated-tau217 and neurofilament light were determined in 159 non-demented individuals, 123 patients with Alzheimer's disease dementia and 35 patients with a non-Alzheimer's dementia from the Swedish BioFINDER-2 study, who underwent longitudinal amyloid (18F-flutemetamol) and tau (18F-RO948) PET, structural MRI (T1-weighted) and cognitive testing. Our univariate linear mixed effect models showed there were several significant associations between the plasma biomarkers with imaging and cognitive measures. However, when all biomarkers were included in the same multivariate linear mixed effect models, we found that increased longitudinal amyloid-PET signals were independently predicted by low baseline plasma Aβ42/40 (P = 0.012), whereas increased tau-PET signals, brain atrophy and worse cognition were independently predicted by high plasma phosphorylated-tau217 (P < 0.004). These biomarkers performed equally well or better than the corresponding biomarkers measured in the CSF. In addition, they showed a similar performance to binary plasma biomarker values defined using the Youden index, which can be more easily implemented in the clinic. In addition, plasma Aβ42/40 and phosphorylated-tau217 did not predict longitudinal changes in patients with a non-Alzheimer's neurodegenerative disorder. In conclusion, our findings indicate that plasma Aβ42/40 and phosphorylated-tau217 could be useful in clinical practice, research and drug development as prognostic markers of future Alzheimer's disease pathology.
Author	Pereira, Joana B Janelidze, Shorena Stomrud, Erik Dage, Jeffrey L van Westen, Danielle Mattsson-Carlgren, Niklas Palmqvist, Sebastian Hansson, Oskar
Author_xml	– sequence: 1 givenname: Joana B orcidid: 0000-0002-3579-8804 surname: Pereira fullname: Pereira, Joana B organization: Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institute, 141 83 Huddinge, Sweden – sequence: 2 givenname: Shorena surname: Janelidze fullname: Janelidze, Shorena organization: Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, SE-20502 Malmö, Sweden – sequence: 3 givenname: Erik surname: Stomrud fullname: Stomrud, Erik organization: Memory Clinic, Skåne University Hospital, 214 28 Malmö, Sweden – sequence: 4 givenname: Sebastian surname: Palmqvist fullname: Palmqvist, Sebastian organization: Memory Clinic, Skåne University Hospital, 214 28 Malmö, Sweden – sequence: 5 givenname: Danielle orcidid: 0000-0001-8649-9874 surname: van Westen fullname: van Westen, Danielle organization: Image and Function, Skåne University Hospital, Malmö 205 02, Sweden – sequence: 6 givenname: Jeffrey L surname: Dage fullname: Dage, Jeffrey L organization: Eli Lilly and Company, Indianapolis, IN 46225, USA – sequence: 7 givenname: Niklas orcidid: 0000-0002-8885-7724 surname: Mattsson-Carlgren fullname: Mattsson-Carlgren, Niklas organization: Wallenberg Center for Molecular Medicine, Lund University, 221 84 Lund, Sweden – sequence: 8 givenname: Oskar surname: Hansson fullname: Hansson, Oskar organization: Memory Clinic, Skåne University Hospital, 214 28 Malmö, Sweden
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/34077494$$D View this record in MEDLINE/PubMed
BookMark	eNpNkLtPwzAYxC1URB8wsiKPDA31I4mTEVW8pEowwEr02f7SuiROiR2h_vcUUSSmu-Gn091Nych3Hgm55OyGs1IudA_OL-ALNM_lCZnwNGeJ4Fk--ufHZBrCljGeSpGfkbFMmVJpmU7I-0sDoQXaQv-BfaC7Hq0zkZoN-DUG6jyFdt90zs5phGFOIfbdbrOn4C013dq76Dr_gx16JRZb9BEtDYPeoonhnJzW0AS8OOqMvN3fvS4fk9Xzw9PydpWYrOAxKWVhbVGArDXWRnLgWha6VDUrteBMGqGUgdqkUmXCZFgao0wBGaASkBklZuT6N3fXd58Dhli1LhhsGvDYDaESmcwLxiRnB_TqiA66RVvtencYv6_-PhHfDLhnRg
CitedBy_id	crossref_primary_10_1093_brain_awad330 crossref_primary_10_1093_brain_awaf033 crossref_primary_10_3389_fnagi_2022_942629 crossref_primary_10_1055_a_1839_6237 crossref_primary_10_1212_WNL_0000000000200118 crossref_primary_10_1038_s41380_022_01531_9 crossref_primary_10_1002_ana_78003 crossref_primary_10_1002_alz_14629 crossref_primary_10_1186_s13195_023_01237_2 crossref_primary_10_1055_a_1726_6361 crossref_primary_10_3390_ijms24065746 crossref_primary_10_1001_jamanetworkopen_2025_0096 crossref_primary_10_1002_alz_14036 crossref_primary_10_1002_alz_14317 crossref_primary_10_1111_eci_70034 crossref_primary_10_12968_hmed_2025_0074 crossref_primary_10_1161_STROKEAHA_122_041854 crossref_primary_10_1002_alz_14397 crossref_primary_10_1002_alz_14430 crossref_primary_10_1186_s13024_024_00750_8 crossref_primary_10_3390_biomedicines10061240 crossref_primary_10_1186_s13195_022_01116_2 crossref_primary_10_1038_s41467_023_42596_6 crossref_primary_10_1186_s12263_023_00722_5 crossref_primary_10_3233_JAD_221287 crossref_primary_10_1002_alz_14318 crossref_primary_10_15252_emmm_202114408 crossref_primary_10_3389_fnagi_2023_1169499 crossref_primary_10_1097_WAD_0000000000000579 crossref_primary_10_1016_j_cca_2022_03_018 crossref_primary_10_3233_JAD_220475 crossref_primary_10_3233_JAD_220673 crossref_primary_10_1002_alz_13157 crossref_primary_10_1177_13872877251372958 crossref_primary_10_1097_CM9_0000000000002566 crossref_primary_10_1136_jnnp_2024_333467 crossref_primary_10_3389_fnagi_2025_1517663 crossref_primary_10_3390_jcm11154515 crossref_primary_10_1016_j_tjpad_2025_100252 crossref_primary_10_1093_aje_kwad197 crossref_primary_10_3233_JAD_215646 crossref_primary_10_1002_alz_70253 crossref_primary_10_1002_alz_14284 crossref_primary_10_1002_alz_14482 crossref_primary_10_1093_brain_awad397 crossref_primary_10_1093_gerona_glaf110 crossref_primary_10_1016_j_ibneur_2023_01_005 crossref_primary_10_1093_braincomms_fcae162 crossref_primary_10_1136_jnnp_2021_328623 crossref_primary_10_1002_VIW_20240119 crossref_primary_10_1002_acn3_51529 crossref_primary_10_1007_s00401_022_02458_9 crossref_primary_10_1016_j_envint_2024_108914 crossref_primary_10_1002_alz_13318 crossref_primary_10_1002_alz_13912 crossref_primary_10_1177_13872877251361354 crossref_primary_10_1002_alz_70504 crossref_primary_10_1002_alz_70625 crossref_primary_10_3390_ijms26157268 crossref_primary_10_3390_biom14010093 crossref_primary_10_1002_ana_27285 crossref_primary_10_1212_WNL_0000000000209307 crossref_primary_10_1016_j_neurobiolaging_2024_08_007 crossref_primary_10_1093_brain_awad267 crossref_primary_10_3389_fnagi_2022_977999 crossref_primary_10_3390_cimb46060304 crossref_primary_10_1002_alz_70465 crossref_primary_10_1177_13872877251333450 crossref_primary_10_1186_s40478_025_02064_2 crossref_primary_10_1093_clinchem_hvac149 crossref_primary_10_1212_WNL_0000000000201479 crossref_primary_10_1002_ctm2_909 crossref_primary_10_1136_jnnp_2021_327788 crossref_primary_10_1212_WNL_0000000000201597 crossref_primary_10_3390_ijms24129797 crossref_primary_10_1038_s41380_025_03166_y crossref_primary_10_1002_alz_13924 crossref_primary_10_1186_s13195_025_01828_1 crossref_primary_10_1002_alz_12756 crossref_primary_10_1002_alz_12959 crossref_primary_10_3233_JAD_221268 crossref_primary_10_1002_alz_13652 crossref_primary_10_1016_j_tjpad_2025_100117 crossref_primary_10_1002_alz_13651 crossref_primary_10_1002_alz_13733 crossref_primary_10_3390_biomedicines10040850 crossref_primary_10_1002_dad2_12487 crossref_primary_10_3390_v16010072 crossref_primary_10_1038_s41398_022_01899_w crossref_primary_10_1186_s13024_022_00533_z crossref_primary_10_1093_gerona_glaf135 crossref_primary_10_1186_s13195_024_01545_1
ContentType	Journal Article
Copyright	The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.
Copyright_xml	– notice: The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.
DBID	CGR CUY CVF ECM EIF NPM 7X8
DOI	10.1093/brain/awab163
DatabaseName	Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic
DatabaseTitle	MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic MEDLINE
Database_xml	– sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	no_fulltext_linktorsrc
Discipline	Medicine
EISSN	1460-2156
ExternalDocumentID	34077494
Genre	Clinical Trial Research Support, Non-U.S. Gov't Journal Article
GroupedDBID	--- -E4 -~X .2P .I3 .XZ .ZR 0R~ 1TH 23N 2WC 4.4 482 48X 53G 5GY 5RE 5VS 5WA 5WD 6PF 70D AABZA AACZT AAIMJ AAJKP AAMDB AAMVS AAOGV AAPNW AAPQZ AAPXW AARHZ AAUAY AAVAP AAVLN AAWTL ABDFA ABEJV ABEUO ABGNP ABIVO ABIXL ABJNI ABKDP ABLJU ABMNT ABNHQ ABNKS ABPTD ABQLI ABQNK ABVGC ABWST ABXVV ABZBJ ACGFS ACIWK ACPRK ACUFI ACUTJ ACUTO ACYHN ADBBV ADEYI ADEZT ADGKP ADGZP ADHKW ADHZD ADIPN ADJQC ADOCK ADQBN ADRIX ADRTK ADVEK ADYVW ADZXQ AEGPL AEJOX AEKSI AELWJ AEMDU AENEX AENZO AEPUE AETBJ AEWNT AFFZL AFGWE AFIYH AFOFC AFXAL AFXEN AGINJ AGKEF AGQXC AGSYK AGUTN AHMBA AHMMS AHXPO AIJHB AJEEA AKWXX ALMA_UNASSIGNED_HOLDINGS ALUQC APIBT APWMN ARIXL ATGXG AXUDD AYOIW BAWUL BAYMD BCRHZ BEYMZ BHONS BQDIO BR6 BSWAC BTRTY BVRKM C45 CDBKE CGR COF CS3 CUY CVF CZ4 DAKXR DIK DILTD DU5 D~K E3Z EBS ECM EE~ EIF EMOBN ENERS F5P F9B FECEO FHSFR FLUFQ FOEOM FOTVD FQBLK GAUVT GJXCC GX1 H13 H5~ HAR HW0 HZ~ IOX J21 J5H JXSIZ KAQDR KBUDW KOP KQ8 KSI KSN L7B M-Z MHKGH ML0 N9A NGC NLBLG NOMLY NOYVH NPM O9- OAUYM OAWHX OBOKY OCZFY ODMLO OHH OJQWA OJZSN OK1 OPAEJ OVD OWPYF P2P PAFKI PEELM PQQKQ Q1. Q5Y R44 RD5 RIG ROL ROX RUSNO RW1 RXO TCURE TEORI TJX TLC TR2 VVN W8F WH7 WOQ X7H YAYTL YKOAZ YSK YXANX ZKX ~91 7X8 ABPQP ABXZS ADNBA AEMQT AFYAG AHGBF AJBYB AJNCP ALXQX
ID	FETCH-LOGICAL-c581t-938dd88a3fbefc31a1b38b97f09b2103c277cafc43752c5e9cc7c8a5ae72a5c72
IEDL.DBID	7X8
ISICitedReferencesCount	98
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000733722200040&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1460-2156
IngestDate	Sun Sep 28 01:34:05 EDT 2025 Wed Feb 19 02:27:17 EST 2025
IsDoiOpenAccess	false
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	9
Keywords	amyloid-β plasma biomarkers cognition MRI PET tau PET
Language	English
License	The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c581t-938dd88a3fbefc31a1b38b97f09b2103c277cafc43752c5e9cc7c8a5ae72a5c72
Notes	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ORCID	0000-0002-3579-8804 0000-0001-8649-9874 0000-0002-8885-7724
OpenAccessLink	http://kipublications.ki.se/Default.aspx?queryparsed=id:148447506
PMID	34077494
PQID	2536800310
PQPubID	23479
ParticipantIDs	proquest_miscellaneous_2536800310 pubmed_primary_34077494
PublicationCentury	2000
PublicationDate	2021-10-22
PublicationDateYYYYMMDD	2021-10-22
PublicationDate_xml	– month: 10 year: 2021 text: 2021-10-22 day: 22
PublicationDecade	2020
PublicationPlace	England
PublicationPlace_xml	– name: England
PublicationTitle	Brain (London, England : 1878)
PublicationTitleAlternate	Brain
PublicationYear	2021
SSID	ssj0014326
Score	2.6354914
Snippet	It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. In...
SourceID	proquest pubmed
SourceType	Aggregation Database Index Database
StartPage	2826
SubjectTerms	Adaptor Proteins, Signal Transducing - blood Adult Aged Aged, 80 and over Amyloid beta-Peptides - blood Atrophy - blood Biomarkers - blood Brain - diagnostic imaging Brain - metabolism Cohort Studies Female Humans Longitudinal Studies Male Middle Aged Neuropsychological Tests Peptide Fragments - blood Predictive Value of Tests
Title	Plasma markers predict changes in amyloid, tau, atrophy and cognition in non-demented subjects
URI	https://www.ncbi.nlm.nih.gov/pubmed/34077494 https://www.proquest.com/docview/2536800310
Volume	144
WOSCitedRecordID	wos000733722200040&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings	1
isFullTextHit
isPrint
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LSwMxEA5qRbz4ftQXETw2tJtHk5xExOKlpQeFniyTx0IP3dbuVv--yTalJ0Hwspds2DCZzcx8M_kGoQfFBWiXG-IVt4SrjiAmaAYBbwxALo2mUDebkIOBGo30MAFuZSqrXJ-J9UHtZjZi5G0qWFfVRJaP808Su0bF7GpqobGNGiy4MlGr5WiTReCMpttFHRJMWzdxbIYgvm1iA4Y2fIPJIgPob95lbWV6h_9d3xE6SP4lflopxDHa8sUJ2uunDPop-hgGd3kKeBrLchYlni_iUIVXF4BLPCkwTEMQP3EtXMGyhSNWHrYCQ-FwqjWaFfG1YlYQV4OL3uFyaSKgU56h997L2_MrST0WiBUqq4hmyjmlgOXG55ZlkBmmjJZ5R5sQDTJLpbSQW86koFZ4ba20CgR4SUFYSc_RTviev0S4S8N-u0wY21FcSw8mj8wymoUYTnQVb6L7teTGQYdjYgIKP1uW443smuhiJf7xfEW2MWYh4pRc86s_zL5G-zSWnATTQukNauThD_a3aNd-VZNycVcrR3gOhv0fqzjGSw
linkProvider	ProQuest
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=Plasma+markers+predict+changes+in+amyloid%2C+tau%2C+atrophy+and+cognition+in+non-demented+subjects&rft.jtitle=Brain+%28London%2C+England+%3A+1878%29&rft.au=Pereira%2C+Joana+B&rft.au=Janelidze%2C+Shorena&rft.au=Stomrud%2C+Erik&rft.au=Palmqvist%2C+Sebastian&rft.date=2021-10-22&rft.eissn=1460-2156&rft.volume=144&rft.issue=9&rft.spage=2826&rft_id=info:doi/10.1093%2Fbrain%2Fawab163&rft_id=info%3Apmid%2F34077494&rft_id=info%3Apmid%2F34077494&rft.externalDocID=34077494
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1460-2156&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1460-2156&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1460-2156&client=summon