Author

Amandine Flaig

Inserm

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Neuroscience· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

Anaïs-Camille Vreulx· 3 shared Devrim KilinciD· 3 shared Jean‐Charles LambertiD· 3 shared Julien ChapuisiD· 3 shared Nicolas Malmanche· 3 shared Philippe AmouyeliD· 3 shared Tiago MendesiD· 3 shared Fanny EysertiD· 2 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersNeuroscience

Anaïs-Camille Vreulx

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3 papers

Recent·Most cited

Alzheimer's genetic risk factor FERMT2 (Kindlin-2) controls axonal growth and synaptic plasticity in an APP-dependent manner.

Fanny Eysert, Audrey Coulon, Emmanuelle Boscher, Anaïs-Camille Vreulx, Amandine Flaig, Tiago Mendes, Sandrine Hughes, Benjamin Grenier‐Boley, Xavier Hanoulle, Florie Demiautte, Charlotte Bauer, Mikael Marttinen, Mari Takalo, Philippe Amouyel, Shruti Desai, , Julien Chapuis

The paper identifies FERMT2 as a key modulator of axon guidance and synaptic plasticity in an APP-dependent manner, linking its genetic risk variant to Alzheimer's disease through miRNA regulation.

Molecular Psychiatry · Nov 3, 2020Peer-reviewedNeuroscience

Pyk2 Overexpression in Postsynaptic Neurons Blocks Aβ1-42-induced Synaptotoxicity in a Microfluidic Co-Culture Model

Devrim Kilinc, Anaïs-Camille Vreulx, Tiago Mendes, Amandine Flaig, Diego Marques Coelho, Maxime Verschoore, Florie Demiautte, Philippe Amouyel, Neuro-CEB Brain Bank, Fanny Eysert, Pierre Dourlen, Julien Chapuis, Marcos R. Costa, Nicolas Malmanche, Frédéric Checler, Jean‐Charles Lambert

The paper develops a microfluidic co-culture model to study Aβ1-42-induced synaptotoxicity and shows Pyk2 overexpression in postsynaptic neurons protects against it.

bioRxiv · Dec 20, 2019 · PreprintNeuroscience

BIN1 recovers tauopathy-induced long-term memory deficits in mice and interacts with Tau through Thr348 phosphorylation

Maxime Sartori, Tiago Mendes, Shruti Desai, Alessia Lasorsa, Adrien Herlédan, Nicolas Malmanche, Petra M. Mäkinen, Mikael Marttinen, Idir Malki, Julien Chapuis, Amandine Flaig, Anaïs-Camille Vreulx, Marion Ciancia, Philippe Amouyel, Florence Leroux, , Jean‐Charles Lambert

This study shows BIN1 overexpression rescues long-term memory deficits in Tau-overexpressing mice and identifies Thr348 phosphorylation as a key regulator of BIN1-Tau interaction.

Acta Neuropathologica · May 7, 2019Peer-reviewedNeuroscience