Quantitative genetics validates previous genetic variants and identifies novel genetic players influencing Alzheimer’s disease cerebrospinal fluid biomarkers
Open accessAbstract
Cerebrospinal fluid (CSF) biomarkers have been extensively investigated in the Alzheimer's disease (AD) field, and are now being applied in clinical practice. CSF amyloid-beta (Aβ1-42), total tau (t-tau), and phosphorylated tau (p-tau) reflect disease pathology, and may be used as quantitative traits for genetic analyses, fostering the identification of new genetic factors and the proposal of novel biological pathways of the disease. In patients, the concentration of CSF Aβ1-42 is decreased due to the accumulation of Aβ1-42 in amyloid plaques in the brain, while t-tau and p-tau levels are increased, indicating the extent of neuronal damage. To better understand the biological mechanisms underlying the regulation of AD biomarkers, and its relation to AD, we examined the association between 36 selected single nucleotide polymorphisms (SNPs) and AD biomarkers Aβ1-42, t-tau, and p-tau in CSF in a cohort of 672 samples (571 AD patients and 101 controls) collected within 10 European consortium centers.Our results highlighted five genes, APOE, LOC100129500, PVRL2, SNAR-I, and TOMM40, previously described as main players in the regulation of CSF biomarkers levels, further reinforcing a role for these in AD pathogenesis. Three new AD susceptibility loci, INPP5D, CD2AP, and CASS4, showed specific association with CSF tau biomarkers. The identification of genes that specifically influence tau biomarkers point out to mechanisms, independent of amyloid processing, but in turn related to tau biology that may open new venues to be explored for AD treatment.
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The CASS4 gene locus has consistently been identified in GWAS studies to be associated with an increased risk of developing AD.
“The CASS4 gene locus has consistently been identified in GWAS studies to be associated with an increased risk of developing AD (Lambert et al., 2013; Lin et al., 2017; Ramos de Matos et al., 2018; Schwartzentruber et al., 2021; Wang et al., 2015b).”
From Alzheimer’s genetic risk factor CASS4 controls microglial focal adhesion biology and amyloidosis (2026) · cites this paper as Ramos de Matos et al., 2018
The Discussion (page unavailable) says a CASS4 variant had previously been associated with AD in a large meta-analysis, supporting the locus’s connection to AD. But it describes that variant as protective, and this study links it to lower tau biomarker levels; it does not establish that the locus was consistently associated with increased AD risk across GWAS studies. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMutations in the focal adhesion gene PTK2B have been linked to increased AD risk in GWAS studies.
“Moreover, mutations in the focal adhesion gene PTK2B , which encodes the protein PYK2 and is a suggested CASS4binding partner (Barrett et al., 2013; Beck et al., 2014), have also been linked to increased AD risk in GWAS studies (Lambert et al., 2013; Lin et al., 2017; Ramos de Matos et al., 2018; Schwartzentruber et al., 2021; Wang et al., 2015b).”
From Alzheimer’s genetic risk factor CASS4 controls microglial focal adhesion biology and amyloidosis (2026) · cites this paper as Ramos de Matos et al., 2018
The Introduction and Discussion passages discuss GWAS findings for other genes, including CD2AP and CASS4, but do not address PTK2B. Searches for “PTK2B” and “PTK2B PYK2 genetic variants increased Alzheimer’s disease risk GWAS” found no passage linking PTK2B variants to increased AD risk. Page numbers were not available in our copy. (LLM, conf=0.74)
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- Authors
- Ramos de Matos, M., Ferreira, C., Herukka, S.-K., Soininen, H., Janeiro, A., Santana, I., Baldeiras, I., Almeida, M. R., Lleó, A., Dols-Icardo, O., Alcolea, D., Benussi, L., Binetti, G., Paterlini, A., Ghidoni, R., Nacmias, B., Meulenbroek, O., van Waalwijk van Doorn, L. J. C., Kuiperi, H. B. J., Hausner, L., Waldemar, G., Simonsen, A. H., Tsolaki, M., Gkatzima, O., Resende de Oliveira, C., Verbeek, M. M., Clarimon, J., Hiltunen, M., de Mendonça, A., & Martins, M.
- Affiliations
- Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
- University of Lisbon (PT)
- University of Eastern Finland (FI)
- Unidade Local de Saúde de Coimbra (PT)
- Universitat Autònoma de Barcelona (ES)
- Department of Neurology and Sant Pau Biomedical Research Institute, Memory Unit, Hospital de la Santa Creu i Sant Pau, Autonomous University of Barcelona, Barcelona, Spain, and Centro de Investigación Biomédica en Red en enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain
- Centro San Giovanni di Dio Fatebenefratelli (IT)
- University of Florence (IT)
- Radboud University Nijmegen (NL)
- Department of Neurology, Department of Laboratory Medicine, Radboud University Medical Centre, Donders institute for Brain, Cognition and Behaviour, Radboud Alzheimer Center, Nijmegen, The Netherlands
- Heidelberg University (DE)
- University of Copenhagen (DK)
- Aristotle University of Thessaloniki (GR)
- Greek Association of Alzheimer's Disease and Related Disorders (GR)
- Neurochemistry Laboratory, CHUC - Centro Hospitalar e Universitário de Coimbra, Neurogenetics Laboratory, CNC - Center for Neuroscience and Cell Biology and CNC.IBILI, Faculty of Medicine, University of Coimbra, Portugal
- Corresponding author
- Martins, Madalena
- ORCID
- Ferreira, Catarina
- Herukka, Sanna-Kaisa
- Soininen, Hilkka
- Janeiro, André
- Santana, Isabel
- Baldeiras, Inês
- Almeida, Maria Rosário
- Lleó, Alberto
- Alcolea, Daniel
- Benussi, Luisa
- Binetti, Giuliano
- Paterlini, Anna
- Ghidoni, Roberta
- Nacmias, Benedetta
- Hausner, Lucrezia
- Waldemar, Gunhild
- Simonsen, Anja Hviid
- Tsolaki, Magda
- Gkatzima, Olymbia
- Verbeek, Marcel M.
- Hiltunen, Mikko
- Martins, Madalena
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2018-10-30
- Volume
- 66
- Issue
- 2
- Pages
- 639-652
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2897394134
- Cited by
- 18
- References
- 32
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 1
- FWCI
- 1.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Florence Research (University of Florence) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
- Funders
- Innovationsfonden
- EU Joint Programme – Neurodegenerative Disease Research
- ZonMw (629000002)
- Academy of Finland (307866)
- Bundesministerium für Bildung und Forschung
- Ministero della Salute
- Sigrid Juséliuksen Säätiö (307866)
- Fundação para a Ciência e a Tecnologia (JPND/0005/2011)
- Instituto de Salud Carlos III
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- Alzheimer's disease, cerebrospinal fluid biomarkers
- MeSH terms
- Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Cytoskeletal Proteins, Female, Genotype, Humans, Male, Middle Aged, Peptide Fragments, Phosphorylation, Genetic Variation, Biomarkers, Amyloid beta-Peptides, tau Proteins, Quantitative Trait Loci, Adaptor Proteins, Signal Transducing
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