ORCID Profile
0000-0001-7624-099X
Current Organisation
Vrije Universiteit Amsterdam
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Publisher: American Physical Society (APS)
Date: 27-05-2020
Publisher: EDP Sciences
Date: 2016
Publisher: American Physical Society (APS)
Date: 09-03-2016
Publisher: EDP Sciences
Date: 2016
Publisher: Elsevier BV
Date: 06-2017
Publisher: Elsevier BV
Date: 11-2017
Publisher: Elsevier BV
Date: 10-2016
Publisher: Cold Spring Harbor Laboratory
Date: 09-03-2022
DOI: 10.1101/2022.03.08.22271043
Abstract: Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer’s disease (AD) more directly than clinical diagnosis. Initiated by the European Alzheimer & Dementia Biobank (EADB), the largest collaborative effort on genetics underlying CSF biomarkers was established, including 31 cohorts with a total of 13,116 in iduals (discovery n = 8,074 replication n = 5,042 in iduals). Besides the APOE locus, novel associations with two other well-established AD risk loci were observed CR1 was shown a locus for amyloid beta 42 (Aβ42) and BIN1 for phosphorylated Tau (pTau). GMNC and C16orf95 were further identified as loci for pTau, of which the latter is novel. Clustering methods exploring the influence of all known AD risk loci on the CSF protein levels, revealed 4 biological categories (amyloid, astrocyte, processing & migration, and migration & motility) suggesting multiple Aβ42 and pTau related biological pathways involved in the etiology of AD. In functional follow-up analyses, GMNC and C16orf95 both associated with lateral ventricular volume, implying an overlap in genetic etiology for tau levels and brain ventricular volume.
Publisher: Springer Science and Business Media LLC
Date: 06-09-2022
DOI: 10.1007/S00401-022-02454-Z
Abstract: Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer’s disease (AD) more directly than clinical diagnosis. Initiated by the European Alzheimer & Dementia Biobank (EADB), the largest collaborative effort on genetics underlying CSF biomarkers was established, including 31 cohorts with a total of 13,116 in iduals (discovery n = 8074 replication n = 5042 in iduals). Besides the APOE locus, novel associations with two other well-established AD risk loci were observed CR1 was shown a locus for Aβ42 and BIN1 for pTau. GMNC and C16orf95 were further identified as loci for pTau, of which the latter is novel. Clustering methods exploring the influence of all known AD risk loci on the CSF protein levels, revealed 4 biological categories suggesting multiple Aβ42 and pTau related biological pathways involved in the etiology of AD. In functional follow-up analyses, GMNC and C16orf95 both associated with lateral ventricular volume, implying an overlap in genetic etiology for tau levels and brain ventricular volume.
No related grants have been discovered for Tetsuya Murakami.