IMPRiND Project

Publishable summaries

IMPRiND produces annual publishable reports which describe the project achievements. They are public and and the latest can be downloaded by clicking on the links below.

IMPRiND Public Events

Below you will find information regarding public events organised by IMPRiND.

Scientific publications

Publications in peer-reviewed journals, conference proceedings, book chapters and books.
1.
Seeding Propensity and Characteristics of Pathogenic αSyn Assemblies in Formalin-Fixed Human Tissue from the Enteric Nervous System, Olfactory Bulb, and Brainstem in Cases Staged for Parkinson’s Disease.
Cells 10, 139 (2021). doi:10.3390/cells10010139
2.
Microglial inclusions and neurofilament light chain release follow neuronal α-synuclein lesions in long-term brain slice cultures.
Molecular Neurodegeneration 16, 54 (2021). doi:10.1186/s13024-021-00471-2
3.
Identification of cis-acting determinants mediating the unconventional secretion of tau.
Scientific Reports 11, 12946 (2021). doi:10.1038/s41598-021-92433-3
4.
The differential solvent exposure of N-terminal residues provides ‘fingerprints’ of alpha-synuclein fibrillar polymorphs.
Journal of Biological Chemistry 100737 (2021). doi:10.1016/j.jbc.2021.100737
5.
Tau assemblies do not behave like independently acting prion-like particles in mouse neural tissue.
Acta Neuropathologica Communications 9, 41 (2021). doi:10.1186/s40478-021-01141-6
6.
TNF-α and α-synuclein fibrils differently regulate human astrocyte immune reactivity and impair mitochondrial respiration.
Cell Reports 34, 108895 (2021). doi:10.1016/j.celrep.2021.108895
7.
Phenotypic manifestation of α-synuclein strains derived from Parkinson’s disease and multiple system atrophy in human dopaminergic neurons.
Nature Communications 12, 3817 (2021). doi:10.1038/s41467-021-23682-z
8.
Overexpression of α-Synuclein by Oligodendrocytes in Transgenic Mice Does Not Recapitulate the Fibrillar Aggregation Seen in Multiple System Atrophy.
Cells 9, 2371 (2020). doi:10.3390/cells9112371
9.
Distinct alpha‐Synuclein species induced by seeding are selectively cleared by the Lysosome or the Proteasome in neuronally differentiated SH‐SY5Y cells.
Journal of Neurochemistry jnc.15174 (2020). doi:10.1111/jnc.15174. Archive: https://zenodo.org/record/4570369#.YD0kCV1KiWh
10.
Structures of α-synuclein filaments from multiple system atrophy.
Nature 585, 464–469 (2020). doi:10.1038/s41586-020-2317-6
11.
Interaction of the chaperones alpha B-crystallin and CHIP with fibrillar alpha-synuclein: Effects on internalization by cells and identification of interacting interfaces.
Biochemical and Biophysical Research Communications 527, 760–769 (2020). doi:10.1016/j.bbrc.2020.04.091
12.
The expression level of alpha-synuclein in different neuronal populations is the primary determinant of its prion-like seeding.
Scientific Reports 10, 4895 (2020). doi:10.1038/s41598-020-61757-x
13.
Novel self-replicating α-synuclein polymorphs that escape ThT monitoring can spontaneously emerge and acutely spread in neurons.
Science Advances 6, eabc4364 (2020). doi:10.1126/sciadv.abc4364
14.
Effects of pharmacological modulators of α-synuclein and tau aggregation and internalization.
Scientific Reports 10, 12827 (2020). doi:10.1038/s41598-020-69744-y
15.
Les protéinopathies infectieuses de Parkinson et d’Alzheimer.
Bulletin de l’Académie Nationale de Médecine 204, 224–231 (2020). doi:10.1016/j.banm.2019.12.019. Archive: https://hal-cea.archives-ouvertes.fr/cea-02859853
16.
Disassembly of Tau fibrils by the human Hsp70 disaggregation machinery generates small seeding-competent species.
Journal of Biological Chemistry 295, 9676–9690 (2020). doi:10.1074/jbc.RA120.013478
17.
Acute targeting of pre-amyloid seeds in transgenic mice reduces Alzheimer-like pathology later in life.
Nature Neuroscience 23, 1580–1588 (2020). doi:10.1038/s41593-020-00737-w. Archive: https://zenodo.org/record/4562254#.YDfVlF1KgdW
18.
The Role of Antibodies and Their Receptors in Protection Against Ordered Protein Assembly in Neurodegeneration.
Frontiers in Immunology 10, 1139 (2019). doi:10.3389/fimmu.2019.01139
19.
Spreading of α-Synuclein and Tau: A Systematic Comparison of the Mechanisms Involved.
Frontiers in Molecular Neuroscience 12, 107 (2019). doi:10.3389/fnmol.2019.00107
20.
α‐synuclein oligomers and fibrils: a spectrum of species, a spectrum of toxicities.
Journal of Neurochemistry 150, 522–534 (2019). doi:10.1111/jnc.14808
21.
LRRK2 modifies α-syn pathology and spread in mouse models and human neurons.
Acta Neuropathologica 137, 961–980 (2019). doi:10.1007/s00401-019-01995-0
22.
Endogenous oligodendroglial alpha-synuclein and TPPP/p25α orchestrate alpha-synuclein pathology in experimental multiple system atrophy models.
Acta Neuropathologica 138, 415–441 (2019). doi:10.1007/s00401-019-02014-y
23.
Reduced serum immunoglobulin G concentrations in multiple sclerosis: prevalence and association with disease-modifying therapy and disease course.
Therapeutic Advances in Neurological Disorders 12, 175628641987834 (2019). doi:10.1177/1756286419878340
24.
Measurement of Tau Filament Fragmentation Provides Insights into Prion-like Spreading.
ACS Chemical Neuroscience 9, 1276–1282 (2018). doi:10.1021/acschemneuro.8b00094
25.
Tau filaments from multiple cases of sporadic and inherited Alzheimer’s disease adopt a common fold.
Acta Neuropathologica 136, 699–708 (2018). doi:10.1007/s00401-018-1914-z

Project Flyer

The IMPRiND project flyer describes the project at a glance. It is mainly intended as a printed product but its electronic version is available for download.

This project receives funding from the Innovative Medicines Initiative 2 Joint Undertaking (www.imi.europa.eu) under grant agreement No 116060. This Joint Undertaking receives support from the European Union’s Horizon 2020 research and innovation programme and EFPIA.

This work is supported by the Swiss State Secretariat for Education‚ Research and Innovation (SERI) under contract number 17.00038.

The opinions expressed and arguments employed herein do not necessarily reflect the official views of these funding bodies.

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