001     277978
005     20250504001140.0
024 7 _ |a 10.1002/alz.70146
|2 doi
024 7 _ |a pmid:40207431
|2 pmid
024 7 _ |a 1552-5260
|2 ISSN
024 7 _ |a 1552-5279
|2 ISSN
024 7 _ |a altmetric:176029093
|2 altmetric
037 _ _ |a DZNE-2025-00510
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Oeckl, Patrick
|0 P:(DE-2719)9001560
|b 0
|e First author
|u dzne
245 _ _ |a Early increase of the synaptic blood marker β-synuclein in asymptomatic autosomal dominant Alzheimer's disease.
260 _ _ |a Hoboken, NJ
|c 2025
|b Wiley
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1745916756_863
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a β-synuclein is a promising blood marker to track synaptic degeneration in Alzheimer's disease (AD) but changes in preclinical AD are unclear.We investigated serum β-synuclein in 69 cognitively unimpaired mutation non-carriers, 78 cognitively unimpaired AD mutation carriers (asymptomatic AD), and 31 symptomatic mutation carriers from the Dominantly Inherited Alzheimer Network.β-synuclein levels were already higher in asymptomatic AD mutation carriers compared to non-carriers and highest in symptomatic carriers. Longitudinal trajectories and correlation analyses indicated that β-synuclein levels start to rise after amyloid deposition preceding axonal degeneration, brain atrophy and hypometabolism, and cognitive decline. β-synuclein levels were associated with cognitive impairment and gradually increased with declining cognition.Our study supports the use of blood β-synuclein to track synaptic changes in preclinical AD and as a surrogate marker for cognitive impairment which might be used in early diagnosis and to support patient selection and monitoring of treatment effects in clinical trials.Blood β-synuclein levels were already higher in asymptomatic Alzheimer's disease (AD) mutation carriers. Blood β-synuclein levels were highest in symptomatic AD mutation carriers. Blood β-synuclein levels start to rise 11 years before symptom onset. Rise of β-synuclein precedes axonal degeneration, brain atrophy, and cognitive decline. β-synuclein levels gradually increased with declining cognition.
536 _ _ |a 353 - Clinical and Health Care Research (POF4-353)
|0 G:(DE-HGF)POF4-353
|c POF4-353
|f POF IV
|x 0
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 1
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a asymptomatic mutation carriers
|2 Other
650 _ 7 |a autosomal dominant Alzheimer´s disease
|2 Other
650 _ 7 |a blood biomarker
|2 Other
650 _ 7 |a preclinical Alzheimer´s disease
|2 Other
650 _ 7 |a synaptic degeneration
|2 Other
650 _ 7 |a β‐synuclein
|2 Other
650 _ 7 |a Biomarkers
|2 NLM Chemicals
650 _ 7 |a beta-Synuclein
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: blood
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Biomarkers: blood
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Mutation: genetics
|2 MeSH
650 _ 2 |a beta-Synuclein: blood
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Brain: diagnostic imaging
|2 MeSH
650 _ 2 |a Synapses
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: blood
|2 MeSH
650 _ 2 |a Longitudinal Studies
|2 MeSH
693 _ _ |0 EXP:(DE-2719)DIAN-20090101
|5 EXP:(DE-2719)DIAN-20090101
|e Longitudinal Study on Dominantly Inherited Alzheimer's Disease
|x 0
700 1 _ |a Mayer, Benjamin
|b 1
700 1 _ |a Bateman, Randall J
|b 2
700 1 _ |a Day, Gregory S
|b 3
700 1 _ |a Fox, Nick C
|b 4
700 1 _ |a Huey, Edward D
|b 5
700 1 _ |a Ibanez, Laura
|b 6
700 1 _ |a Ikeuchi, Takeshi
|b 7
700 1 _ |a Jucker, Mathias
|0 P:(DE-2719)2000010
|b 8
|u dzne
700 1 _ |a Lee, Jae-Hong
|0 P:(DE-HGF)0
|b 9
700 1 _ |a Levin, Johannes
|0 P:(DE-2719)2811659
|b 10
|u dzne
700 1 _ |a Llibre-Guerra, Jorge J
|b 11
700 1 _ |a Lopera, Francisco
|b 12
700 1 _ |a McDade, Eric
|b 13
700 1 _ |a Morris, John C
|b 14
700 1 _ |a Niimi, Yoshiki
|b 15
700 1 _ |a Roh, Jee Hoon
|b 16
700 1 _ |a Sánchez-Valle, Raquel
|b 17
700 1 _ |a Schofield, Peter R
|b 18
700 1 _ |a Otto, Markus
|0 0000-0003-4273-4267
|b 19
700 1 _ |a Network, Dominantly Inherited Alzheimer
|b 20
|e Collaboration Author
773 _ _ |a 10.1002/alz.70146
|g Vol. 21, no. 4, p. e70146
|0 PERI:(DE-600)2201940-6
|n 4
|p e70146
|t Alzheimer's and dementia
|v 21
|y 2025
|x 1552-5260
856 4 _ |u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP1.xlsx
856 4 _ |u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP2.pdf
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/277978/files/DZNE-2025-00510.pdf
856 4 _ |u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP1.csv
856 4 _ |u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP1.ods
856 4 _ |u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP1.xls
856 4 _ |x pdfa
|u https://pub.dzne.de/record/277978/files/DZNE-2025-00510%20SUP2.pdf?subformat=pdfa
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/277978/files/DZNE-2025-00510.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:277978
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9001560
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 8
|6 P:(DE-2719)2000010
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 10
|6 P:(DE-2719)2811659
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-353
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Clinical and Health Care Research
|x 0
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 1
914 1 _ |y 2025
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2025-01-06
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2025-01-06
915 _ _ |a Creative Commons Attribution CC BY 4.0
|0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b ALZHEIMERS DEMENT : 2022
|d 2025-01-06
915 _ _ |a DEAL Wiley
|0 StatID:(DE-HGF)3001
|2 StatID
|d 2025-01-06
|w ger
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2025-01-06
915 _ _ |a IF >= 10
|0 StatID:(DE-HGF)9910
|2 StatID
|b ALZHEIMERS DEMENT : 2022
|d 2025-01-06
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2025-01-06
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2025-01-06
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
|d 2025-01-06
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2025-01-06
920 1 _ |0 I:(DE-2719)5000073
|k AG Öckl
|l Translational Mass Spectrometry and Biomarker Research
|x 0
920 1 _ |0 I:(DE-2719)1210001
|k AG Jucker
|l Cell Biology of Neurological Diseases
|x 1
920 1 _ |0 I:(DE-2719)1111016
|k AG Levin
|l Clinical Neurodegeneration
|x 2
920 1 _ |0 I:(DE-2719)1111015
|k Clinical Research (Munich)
|l Clinical Research (Munich)
|x 3
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)5000073
980 _ _ |a I:(DE-2719)1210001
980 _ _ |a I:(DE-2719)1111016
980 _ _ |a I:(DE-2719)1111015
980 1 _ |a FullTexts


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21