Author

Mathias De Decker

VIB-KU Leuven Center for Brain & Disease ResearchORCID 0000-0002-0966-3770Unclaimed 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:human· 2 Research Focus:cell type annotation· 1 Organism:Drosophila· 1 Assay:proteomics· 1

Frequent Co-Authors

Ludo Van Den BoschiD· 2 shared Matthieu MoisseiD· 2 shared Philip Van DammeiD· 2 shared Aaron D. GitleriD· 1 shared Alexander McCampbelliD· 1 shared Ann Swijsen· 1 shared Arpan R. MehtaiD· 1 shared Bhuvaneish Thangaraj SelvarajiD· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersNeuroscience

Ludo Van Den BoschORCID

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2 papers

Recent·Most cited

NeurosciencebioRxivPreprintFeb 28, 2022

C21orf2 mutations found in ALS disrupt primary cilia function

Mathias De Decker, Pavol Zelina, Thomas G. Moens…·Philip Van Damme

This study identifies C21orf2 mutations in ALS as causing cilia dysfunction and impaired sonic hedgehog signaling in motor neurons.

5 citations

humanproteomics

𝕏 PostBluesky

NeuroscienceScience AdvancesPeer-reviewedApr 9, 2021

C9orf72-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility

Laura Fumagalli, Florence L. Young, Steven Boeynaems…·Philip Van Damme

This study shows that C9orf72 repeat expansions produce toxic arginine-rich DPRs that disrupt axonal transport by interacting with microtubules and motor proteins, contributing to ALS/FTD.

95 citationstop 2%

humanDrosophila

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