Functional screening of Alzheimer risk loci identifies PTK2B as an in vivo modulator and early marker of Tau pathology
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A recent genome-wide association meta-analysis for Alzheimer's disease (AD) identified 19 risk loci (in addition to APOE) in which the functional genes are unknown. Using Drosophila, we screened 296 constructs targeting orthologs of 54 candidate risk genes within these loci for their ability to modify Tau neurotoxicity by quantifying the size of >6000 eyes. Besides Drosophila Amph (ortholog of BIN1), which we previously implicated in Tau pathology, we identified p130CAS (CASS4), Eph (EPHA1), Fak (PTK2B) and Rab3-GEF (MADD) as Tau toxicity modulators. Of these, the focal adhesion kinase Fak behaved as a strong Tau toxicity suppressor in both the eye and an independent focal adhesion-related wing blister assay. Accordingly, the human Tau and PTK2B proteins biochemically interacted in vitro and PTK2B co-localized with hyperphosphorylated and oligomeric Tau in progressive pathological stages in the brains of AD patients and transgenic Tau mice. These data indicate that PTK2B acts as an early marker and in vivo modulator of Tau toxicity.
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Genetic screens identified p130CAS, Fak, Eph, Rab3-GEF, cindr, Fit1, Aret and Rhea, orthologs of CASS4, PTK2B, EPHA1, MADD, CD2AP, FERMT2, CELF1 and TLN2, as modulators of Tau toxicity.
“Beyond BIN1, this approach identified p130CAS, Fak, Eph, Rab3-GEF, cindr, Fit1, Aret and Rhea respective orthologs of CASS4, PTK2B, EPHA1, MADD, CD2AP, FERMT2, CELF1 and TLN2 [26, 42, 119].”
From The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis? (2019) · cites this paper as [26]
The Results section (page not supplied) identifies p130CAS/CASS4, Fak/PTK2B, Eph/EPHA1 and Rab3-GEF/MADD as Tau-toxicity modulators. The Discussion says this screen found no positive hits for the CD2AP and FERMT2 loci, attributes the suggestion about aret/CELF1 to another screen, and does not identify Rhea/TLN2 as a hit. Thus this source supports only part of the cited list. (LLM, conf=0.89)
Experimental — accuracy not yet measuredPyk2 accumulates early in the somata of neurons exhibiting Tau pathology in AD patients and in a mouse model.
“Pyk2 (product of PTK2B) has been further shown to accumulate early in the somata of neurons exhibiting Tau pathology in AD patients and in a mouse model [26].”
From The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis? (2019) · cites this paper as [26]
A genetic interaction between Pyk2 and Tau was detected.
“As mentioned earlier, we were able to detect a genetic interaction between Pyk2 and Tau [26].”
From The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis? (2019) · cites this paper as [26]
For previously reported loci, applying the same prioritization approach highlights several genes involved in APP metabolism (FERMT2, PICALM) or tau toxicity (BIN1, CD2AP, FERMT2, CASS4, PTK2B).
“For previously reported loci, applying the same prioritization approach highlights several genes, as described in Fig. 2, some of which are involved in APP metabolism (FERMT2, PICALM) or tau toxicity (BIN1, CD2AP, FERMT2, CASS4, PTK2B)98–101.”
From Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing (2019) · cites this paper as [98]
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- Authors
- Dourlen, P., Fernandez-Gomez, F. J., Dupont, C., Grenier-Boley, B., Bellenguez, C., Obriot, H., Caillierez, R., Sottejeau, Y., Chapuis, J., Bretteville, A., Abdelfettah, F., Delay, C., Malmanche, N., Soininen, H., Hiltunen, M., Galas, M.-C., Amouyel, P., Sergeant, N., Buée, L., Lambert, J.-C., & Dermaut, B.
- Affiliations
- Inserm (FR)
- University of Eastern Finland (FI)
- Corresponding author
- Dourlen, P
- Lambert, J-C
- Dermaut, B
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2016-04-26
- Volume
- 22
- Issue
- 6
- Pages
- 874-883
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC5444024
- OpenAlex
- W2342749204
- Cited by
- 118
- References
- 39
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 7 · 2023: 11 · 2022: 13 · 2021: 14 · 2020: 7 · 2019: 23 · 2018: 14 · 2017: 13 · 2016: 2
- FWCI
- 13.94
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Psychiatry (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- UEF eRepo (University of Eastern Finland) (submittedVersion, cc-by)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion, cc-by)
- Funders
- Alzheimer's Association (BFG-14-318355)
- Itä-Suomen Yliopisto
- Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer's disease
- European Commission (305299, 601055)
- Agence Nationale de la Recherche (ANR-11-LABX-0009)
- Academy of Finland (V16001)
- Belgian Federal Science Policy Office (P7/16)
- Fondation pour la Recherche Médicale
- Kuopion Yliopistollinen Sairaala (VTR grant V16001, V16001)
- Centre National de la Recherche Scientifique
- Sigrid Juséliuksen Säätiö
- National Institutes of Health (NIH P40OD018537, P40OD018537)
- National Institute of General Medical Sciences (R01GM084947, GM084947)
- Institute of Genetics
- 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 › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, Pyk2, focal adhesion kinase, tau pathology, tau toxicity, Drosophila, functional screening, BIN1, EphA1, MADD, hyperphosphorylated tau, early biomarkers
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Drosophila, Humans, Risk Factors, Biomarkers, tau Proteins, Genetic Predisposition to Disease, Focal Adhesion Kinase 2, Genome-Wide Association Study, Genetic Loci
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