Alzheimer’s genetic risk factor FERMT2 (Kindlin-2) controls axonal growth and synaptic plasticity in an APP-dependent manner
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Abstract
Although APP metabolism is being intensively investigated, a large fraction of its modulators is yet to be characterized. In this context, we combined two genome-wide high-content screenings to assess the functional impact of miRNAs and genes on APP metabolism and the signaling pathways involved. This approach highlighted the involvement of FERMT2 (or Kindlin-2), a genetic risk factor of Alzheimer’s disease (AD), as a potential key modulator of axon guidance, a neuronal process that depends on the regulation of APP metabolism. We found that FERMT2 directly interacts with APP to modulate its metabolism, and that FERMT2 underexpression impacts axonal growth, synaptic connectivity, and long-term potentiation in an APP-dependent manner. Last, the rs7143400-T allele, which is associated with an increased AD risk and localized within the 3′UTR of FERMT2, induced a downregulation of FERMT2 expression through binding of miR-4504 among others. This miRNA is mainly expressed in neurons and significantly overexpressed in AD brains compared to controls. Altogether, our data provide strong evidence for a detrimental effect of FERMT2 underexpression in neurons and insight into how this may influence AD pathogenesis.
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Synaptic fragility/sensitivity was proposed as a pathological trigger depending on genetic risk factors, some of which have already been linked to synaptic mechanisms such as BIN1, FERMT2, PTK2B or CD2AP.
“we proposed synaptic fragility/sensitivity as a pathological trigger10, depending on genetic risk factors, some of which have already been linked to synaptic mechanisms, such as BIN1, FERMT2, PTK2B or CD2AP9–12.”
From PLCG2 downregulation impairs synaptic function and increases Alzheimer’s disease hallmarks in neuronal cultures (2026) · cites this paper as [10]
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“Based on this new genetic landscape of AD, and beyond inflammation processes 9 , we proposed synaptic fragility/sensitivity as a pathological trigger 10 , depending on genetic risk factors, some of which have already been linked to synaptic mechanisms, such as BIN1 , FERMT2 , PTK2B or CD2AP 9–12 .”
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- Authors
- Eysert, F., Coulon, A., Boscher, E., Vreulx, A.-C., Flaig, A., Mendes, T., Hughes, S., Grenier-Boley, B., Hanoulle, X., Demiautte, F., Bauer, C., Marttinen, M., Takalo, M., Amouyel, P., Desai, S., Pike, I., Hiltunen, M., Chécler, F., Farinelli, M., Delay, C., Malmanche, N., Hébert, S. S., Dumont, J., Kilinc, D., Lambert, J.-C., & Chapuis, J.
- Affiliations
- Inserm (FR)
- Centre hospitalier de l'Université Laval (CA)
- E-Phy-Science (France) (FR)
- Centre National de la Recherche Scientifique (FR)
- University of Eastern Finland (FI)
- Proteome Sciences (United Kingdom) (GB)
- Corresponding author
- Chapuis, Julien
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2020-11-03
- Volume
- 26
- Issue
- 10
- Pages
- 5592-5607
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC8758496
- OpenAlex
- W3094899843
- Cited by
- 55
- References
- 65
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 16 · 2023: 11 · 2022: 8 · 2021: 3 · 2019: 1
- FWCI
- 3.31
- Type
- journal article
- Language
- en
- Update notices
- correction (2021-01-04)
- Open access
- hybrid
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- Funders
- Itä-Suomen Yliopisto
- EU Joint Programme – Neurodegenerative Disease Research (3DMiniBrain)
- Fondation Vaincre Alzheimer (FR-17006p)
- Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer's disease
- Equipex
- Agence Nationale de la Recherche (ANR-11-LABX-0009)
- Institut National de la Santé et de la Recherche Médicale
- Sigrid Juséliuksen Säätiö (307866)
- Conseil Régional Hauts-de-France
- FONDATION ALZHEIMER
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- FERMT2, Kindlin-2, Alzheimer's disease, APP metabolism, axon growth, axon guidance, synaptic plasticity, long-term potentiation, synaptic connectivity, microRNA regulation, 3' untranslated region, protein-protein interaction, genetic risk factors, high-content screening
- MeSH terms
- Alzheimer Disease, Humans, Membrane Proteins, Neoplasm Proteins, Neuronal Plasticity, Neurons, Risk Factors, Amyloid beta-Protein Precursor
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