Author

Leonardo Nardi

University Medical Center of the Johannes Gutenberg University MainzORCID 0000-0001-8802-1065Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

Michael J. SchmeißeriD· 2 shared Ali AbdollahzadehiD· 1 shared Andrea Conrad· 1 shared Andrea HellwigiD· 1 shared Andreas BaueriD· 1 shared Andreas DaiberiD· 1 shared Andreas S. ReichertiD· 1 shared Angela OskampiD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersNeuroscience

Michael J. SchmeißerORCID

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2 papers

Recent·Most cited

Glucocorticoids target postnatal oligodendrocyte precursor cells to modulate adult hippocampal network plasticity and stress-induced behavior

Lorenzo Mattioni, Giulia Poggi, Celine Gallagher, Katrin Becker, Linh Le, Maja Papic, Jasmin Engbers, Maija-Kreetta Koskinen, Ali Abdollahzadeh, David P. Herzog, Leonardo Nardi, Andrea Conrad, Sarah Winterberg, Christa Merte-Grebe, Liana Melo-Thomas, , Giulia Treccani

This study shows that deleting glucocorticoid receptors in postnatal oligodendrocyte precursor cells reduces oligodendrocyte density, alters hippocampal activity, and impairs memory in adult mice.

Proceedings of the National Academy of Sciences · Jul 20, 2026Peer-reviewedNeuroscience

NECAB2 participates in an endosomal pathway of mitochondrial stress response at striatal synapses

Diones Bueno, Partha Narayan Dey, Teresa Schacht, Christina Wolf, Verena Wüllner, Elena Morpurgo, Liliana Rojas-Charry, Lena Sessinghaus, Petra Leukel, Clemens Sommer, Konstantin Radyushkin, Michael K. E. Schäfer, Luise Florin, Jan Baumgart, Paul Stamm, , Axel Methner

This study identifies NECAB2's role in an endosomal pathway for mitochondrial stress response and repair in striatal synapses, linking its loss to synaptic loss and behavioral deficits.

bioRxiv · Feb 15, 2021 · PreprintNeuroscience