![#](https://www.bordeaux-neurocampus.fr/wp-content/uploads/2018/07/florent-laferriere-630x779.jpg)
Florent Laferrière
Chercheur
CR / CNRS/ Contact
+33 5 33 51 47 97
www.orcid.org/0000-0002-0753-5505
/ Adresse
IMN - UMR 5293 - CNRS/Université de Bordeaux - Centre Broca Nouvelle-Aquitaine – 3e étage - 146 rue Léo-Saignat- CS 61292 – Case 28 - 33076 Bordeaux cedex - France
![](https://www.bordeaux-neurocampus.fr/wp-content/uploads/2018/07/florent-laferriere.jpg)
Publications
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Biases in α-synuclein immuno-quantitation: a core problem for basic and ancillary studies of Parkinson’s disease and multiple system atrophy
Transl Neurodegener. 2024-03-25. 13(1)
10.1186/s40035-024-00408-x -
A model of human neural networks reveals NPTX2 pathology in ALS and FTLD
Nature. 2024-02-14.
10.1038/s41586-024-07042-7 -
Reconsidering α-Synuclein inclusion pathology in neurons, mice, and humans with an antibody sensing NAC engagement during α-Synuclein amyloid conversion
Preprint - Research Square. 2024-02-07.
10.21203/rs.3.rs-3921168/v1 -
Oligodendrocytes Prune Axons Containing α-Synuclein Aggregates In Vivo: Lewy Neurites as Precursors of Glial Cytoplasmic Inclusions in Multiple System Atrophy?
biomolecules. 2023-02-01. 13(2) : 269.
10.3390/biom13020269 -
Neurons with Cat’s Eyes: A Synthetic Strain of α-Synuclein Fibrils Seeding Neuronal Intranuclear Inclusions
Biomolecules. 2022-03-11. 12(3) : 436.
10.3390/biom12030436 -
Similar neuronal imprint and no cross-seeded fibrils in α-synuclein aggregates from MSA and Parkinson’s disease
npj Parkinsons Dis.. 2022-01-13. 8(1)
10.1038/s41531-021-00264-w -
Human neural networks with sparse TDP-43 pathology reveal NPTX2 misregulation in ALS/FTLD
. 2021-12-09.
10.1101/2021.12.08.471089 -
Similar neuronal imprint and absence of cross-seeded partner fibrils in α-synuclein aggregates from MSA and Parkinson’s disease brains
Preprint bioRxiv. 2021-06-22.
10.1101/2021.06.22.449410 -
Overexpression of α-Synuclein by Oligodendrocytes in Transgenic Mice Does Not Recapitulate the Fibrillar Aggregation Seen in Multiple System Atrophy
Cells. 2020-10-29. 9(11) : 2371.
10.3390/cells9112371 -
Novel self-replicating α-synuclein polymorphs that escape ThT monitoring can spontaneously emerge and acutely spread in neurons
Sci. Adv.. 2020-10-01. 6(40) : eabc4364.
10.1126/sciadv.abc4364 -
Novel self-replicating α-synuclein polymorphs that escape ThT monitoring can spontaneously emerge and acutely spread in neurons
Sci. Adv.. 2020-10-01. 6(40) : eabc4364.
10.1126/sciadv.abc4364 -
Identification of distinct pathological signatures induced by patient-derived α-synuclein structures in nonhuman primates
Sci. Adv.. 2020-05-01. 6(20) : eaaz9165.
10.1126/sciadv.aaz9165 -
Crossing Species Barriers Relies on Structurally Distinct Prion Assemblies and Their Complementation
Mol Neurobiol. 2020-04-01. 57(6) : 2572-2587.
10.1007/s12035-020-01897-3 -
Targeting α-synuclein for PD Therapeutics: A Pursuit on All Fronts
Biomolecules. 2020-03-03. 10(3) : 391.
10.3390/biom10030391 -
Emergence of stealth polymorphs that escape α-synuclein amyloid monitoring, take over and acutely spread in neurons
. 2020-02-12.
10.1101/2020.02.11.943670 -
Complementation between pathological prion protein subassemblies to cross existing species barriers
. 2019-12-03.
10.1101/861278 -
Identification of distinct pathological signatures induced by patient-derived α-synuclein structures in non-human primates
. 2019-10-31.
10.1101/825216 -
Early stage prion assembly involves two subpopulations with different quaternary structures and a secondary templating pathway
Commun Biol. 2019-10-04. 2(1)
10.1038/s42003-019-0608-y -
Quaternary structural convergence and structural diversification of prion assemblies at the early replication stage
. 2019-03-20.
10.1101/583781 -
SarkoSpin: A Technique for Biochemical Isolation and Characterization of Pathological TDP-43 Aggregates
BIO-PROTOCOL. 2019-01-01. 9(22)
10.21769/bioprotoc.3424 -
TDP-43 extracted from frontotemporal lobar degeneration subject brains displays distinct aggregate assemblies and neurotoxic effects reflecting disease progression rates.
Nat Neurosci. 2018-12-17. 22(1) : 65-77.
10.1038/s41593-018-0294-y -
Memory Decline and Its Reversal in Aging and Neurodegeneration Involve miR-183/96/182 Biogenesis
Mol Neurobiol. 2018-08-20.
10.1007/s12035-018-1314-3 -
Hypertonic Stress Causes Cytoplasmic Translocation of Neuronal, but Not Astrocytic, FUS due to Impaired Transportin Function
Cell Reports. 2018-07-01. 24(4) : 987-1000.e7.
10.1016/j.celrep.2018.06.094 -
Crystal structure of TDP-43 N-terminal domain at 2.1 A resolution
. 2017-07-05.
10.2210/pdb5mdi/pdb -
Functional and dynamic polymerization of the ALS-linked protein TDP-43 antagonizes its pathologic aggregation
Nat Commun. 2017-06-29. 8(1)
10.1038/s41467-017-00062-0 -
Protease resistance of infectious prions is suppressed by removal of a single atom in the cellular prion protein.
PLoS ONE. 2017-02-16. 12(2) : e0170503.
10.1371/journal.pone.0170503 -
Advances and challenges in understanding the multifaceted pathogenesis of amyotrophic lateral sclerosis.
Swiss Med Wkly. 2015-01-30.
10.4414/smw.2015.14054 -
Highly infectious prions generated by a single round of microplate-based protein misfolding cyclic amplification.
mBio. 2013-12-31. 5(1)
10.1128/mbio.00829-13 -
Quaternary Structure of Pathological Prion Protein as a Determining Factor of Strain-Specific Prion Replication Dynamics
PLoS Pathog. 2013-10-10. 9(10) : e1003702.
10.1371/journal.ppat.1003702