Picture of posters from convention
 

 Posters 

ALZHEIMER'S DISEASE

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N6P33

NSP19 an original green-extract from Dioscorea villosa with neuroprotective effects in in vitro Alzheimer’s disease models.

RFMF - Toulouse (France) - Jan 2020

#AD

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N6P27

Tau Site-specific hyperphosphorylation by Aβ oligomers and glutamate in a primary culture of cortical neurons.

AAIC 2019 - Los Angeles (USA) - July 2019

#AD

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N6P21

From traditional use to standardized neuroprotective green-extract of Huperzia serrata.

CNP 2018 - Athens (Greece) - Nov 2018

#AD

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N6P16

ER-stress regulation and effect of Guanabenz in primary cortical neurons injured with Aβ1-42 peptide, an in vitro model of Alzheimer’s disease.

SDN - Strasbourg (France) - June 2018

#AD

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N6P10

Mode of action study of NSP01-E, a potential treatment for Alzheimer’s disease, in protection against amyloid β peptide (Aβ) injury.

AAIC 2016 - Toronto (Canada) - July 2016

#AD

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N6P02

Beta-estradiol protects cortical neurons from beta-amyloid oligomers toxicity through mediations of the Ras/raf and PI3K pathways.

SFN 2014 - Washington - Nov 2014

#AD

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N6P29

Neuroprotective activity of NSP06: an ecofriendly plant extract from Verbena officinalis.

Phyt'Arom - Grasse (France) - Oct 2019

#AD

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N6P25

Neuroprotective activity of NSP06: an ecofriendly plant extract from Verbena officinalis.

Metasud - Toulon (France) - June 2019

#AD

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N6P20

Activation of the PERK pathway reduces the proteinopathy associated with neurodegenerative diseases: evidence from in vitro models of AD, PD and ALS.

4th  annual Neuroscience R&D Technologies Conference - Munich (Germany) - Oct 2018

#AD, #PD, #ALS

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N6P14

Effects of circulating and neuronal amyloid peptide oligomers on the BBB integrity: Consequences on the neurodegeneration process.

AAIC 2017 - London (UK) - July 2017

#AD, #BBB

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N6P05

Neurodegeneration induced by Aβ oligomeric fractions: Role of NMDA receptors and mGluR5.

AD/PD - Geneva (Switzerland) - March 2015

#AD

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N6P28

From traditional use to NSP01: a standardized neuroprotective green-extract of Huperzia serrata.

Phyt'Arom - Grasse (France) - Oct 2019

#AD

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N6P23

Effect of DAPK1 inhibition on

site-specific hyperphosphorylation of Tau protein in two in vitro models of Alzheimer’s disease.

AD/PD 2019 - Lisbon (Portugal) - March 2019

#AD

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N6P17

A new treatment for Alzheimer’s disease: AZP2006 prevents and reverses amyloid and Tau damages via release of one growth factor and reduction of neuroinflammation.

AAT-AD/PD - Torino (Italy) - March 2018

#AD

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N6P11

A novel triple cell co-culture model for mimicking the BBB into normal or pathological situations.

2nd annual Neuroscience R&D Technologies Conference - London (UK) - Sep 2016

#AD, #BBB

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N6P04

NSP01-E01 and NSP01-C01: New preparations able to protect from beta-amyloid (Aβ) injuries. Ptential treatments for Alzheimer's disease.

ARUK Conference - London (UK) - March 2015

#AD

 
 

PARKINSON'S DISEASE

 

AMYOTROPHIC LATERAL SCLEROSIS

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N6P32

Effects of riluzole and edaravone in SOD1 and WT spinal motor neurons injured with glutamate: a comparative study.

BPS 2019 - Edinburgh (UK) - Dec 2019

#ALS

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N6P12

Amyloid peptide and cytoplasmic TDP-43 accumulation in pathogenesis of ALS: an in vitro study.

AD/PD 2015 - Vienna (Austria) - March 2015

#ALS

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N6P01

Role of β-Amyloid (Aβ) Oligomeric fractions in ALS disease.

ICNMD - Nice (France) - June 2014

#ALS

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N6P24

Translocation of TDP-43 and FUS in SOD1 Tg and WT spinal cord motor neurons injured with glutamate or AβO1-42 peptide: in vitro models of ALS.

NeuroFrance - Marseille (France) - May 2019

#ALS

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N6P09

Pathological role of amyloid peptide in neuromuscular disease, glutamate and glucose involvement.

Myology 2016 - Lyon (France) - March 2016

#ALS

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N6P20

Activation of the PERK pathway reduces the proteinopathy associated with neurodegenerative diseases: evidence from in vitro models of AD, PD and ALS.

4th  annual Neuroscience R&D Technologies Conference - Munich (Germany) - Oct 2018

#AD, #PD, #ALS

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N6P08

Deleterious effects of amyloid beta peptide in the neuromuscular junction: consequences in ALS disease.

JSFM - Lyon (France) - Nov 2015

#ALS

CHEMOTHERAPY-INDUCED PERIPHERAL NEUROPATHY

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N6P26

The Chemotherapy-induced peripheral neuropathy involves specific neural or Schwann cell targets. The case of Cisplatin, Taxol and Vincristine.

PNS - Genoa (Italy) - June 2019

#CIPN

BLOOD BRAIN BARRIER

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N6P15

Effects of circulating and neuronal amyloid peptide oligomers on BBB integrity: consequences for the disease.

3rd annual Neuroscience R&D Technologies Conference - London (UK) - Sep 2017 

#BBB

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N6P14

Effects of circulating and neuronal amyloid peptide oligomers on the BBB integrity: Consequences on the neurodegeneration process.

AAIC 2017 - London (UK) - July 2017

#AD, #BBB

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N6P11

A novel triple cell co-culture model for mimicking the BBB into normal or pathological situations.

2nd annual Neuroscience R&D Technologies Conference - London (UK) - Sep 2016

#AD, #BBB

 Publications 

Ambroxol Hydrochloride Improves Motor Functions and Extends Survival in a Mouse Model of Familial Amyotrophic Lateral Sclerosis.

Alexandra Bouscary, Cyril Quessada, Althéa Mosbach, Noëlle Callizot, Michael Spedding, Jean-Philippe Loeffler, Alexandre Henriques.

 

Published: August 7, 2019.

 

Abstract

Amyotrophic lateral sclerosis (ALS) is a multifactorial and fatal neurodegenerative disease. Growing evidence connects sphingolipid metabolism to the pathophysiology of ALS. In particular, levels of ceramides, glucosylceramides, and gangliosides are dysregulated in the central nervous system and at the neuromuscular junctions of both animal models and patients. Glucosylceramide is the main precursor of complex glycosphingolipids that is degraded by lysosomal (GBA1) or non-lysosomal (GBA2) glucocerebrosidase. Here, we report that GBA2, but not GBA1, activity is markedly increased in the spinal cord, of SOD1G86R mice, an animal model of familial ALS, even before disease onset. We therefore investigated the effects of ambroxol hydrochloride, a known GBA2 inhibitor, in SOD1G86R mice. A presymptomatic administration of ambroxol hydrochloride, in the drinking water, delayed disease onset, protecting neuromuscular junctions, and the number of functional spinal motor neurons. When administered at disease onset, ambroxol hydrochloride delayed motor function decline, protected neuromuscular junctions, and extended overall survival of the SOD1G86R mice. In addition, ambroxol hydrochloride improved motor recovery and muscle re-innervation after transient sciatic nerve injury in non-transgenic mice and promoted axonal elongation in an in vitro model of motor unit. Our study suggests that ambroxol hydrochloride promotes and protects motor units and improves axonal plasticity, and that this generic compound is a promising drug candidate for ALS.

https://www.frontiersin.org/articles/10.3389/fphar.2019.00883/full

Necrosis, apoptosis, necroptosis, three modes of action of dopaminergic neuron neurotoxins.

Noelle Callizot, Maud Combes, Alexandre Henriques, Philippe Poindron.

 

Published: April 25, 2019.

 

Abstract
Most of the Parkinson’s disease (PD) cases are sporadic, although several genes are directly related to PD. Several pathways are central in PD pathogenesis : protein aggregation linked to proteasomal impairments, mitochondrial dysfunctions and impairment in dopamine (DA) release. Here we studied the close crossing of mitochondrial dysfunction and aggregation of α-synuclein (α-syn) and in the extension in the dopaminergic neuronal death. Here, using rat primary cultures of mesencephalic neurons, we induced the mitochondrial impairments using “DA-toxins” (MPP+, 6OHDA, rotenone). We showed that the DA-Toxins induced dopaminergic cell death through different pathways : caspase-dependent cell death for 6OHDA ; MPP+ stimulated caspase-independent cell death, and rotenone activated both pathways. In addition, a decrease in energy production and/or a development of oxidative stress were observed and were linked to α-syn aggregation with generation of Lewy body-like inclusions (found inside and outside the dopaminergic neurons). We demonstrated that any of induced mitochondrial disturbances and processes of death led to α-syn protein aggregation and finally to cell death. Our study depicts the cell death mechanisms taking place in in vitro models of Parkinson’s disease and how mitochondrial dysfunctions is at the cross road of the pathologies of this disease.

https://doi.org/10.1371/journal.pone.0215277

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing.

Boland B, Yu WH, Corti O, Mollereau B, Henriques A, Bezard E, Pastores GM, Rubinsztein DC, Nixon RA, Duchen MR, Mallucci GR, Kroemer G, Levine B, Eskelinen EL, Mochel F, Spedding M, Louis C, Martin OR, Millan MJ.

 

Nat Rev Drug Discov. 2018 Sep ;17(9):660-688. doi : 10.1038/nrd.2018.109. Epub 2018 Aug 17.

Abstract

Neurodegenerative disorders of ageing (NDAs) such as Alzheimer disease, Parkinson disease, frontotemporal dementia, Huntington disease and amyotrophic lateral sclerosis represent a major socio-economic challenge in view of their high prevalence yet poor treatment. They are often called ’proteinopathies’ owing to the presence of misfolded and aggregated proteins that lose their physiological roles and acquire neurotoxic properties. One reason underlying the accumulation and spread of oligomeric forms of neurotoxic proteins is insufficient clearance by the autophagic-lysosomal network. Several other clearance pathways are also compromised in NDAs : chaperone-mediated autophagy, the ubiquitin-proteasome system, extracellular clearance by proteases and extrusion into the circulation via the blood-brain barrier and glymphatic system. This article focuses on emerging mechanisms for promoting the clearance of neurotoxic proteins, a strategy that may curtail the onset and slow the progression of NDAs.

https://www.ncbi.nlm.nih.gov/pubmed/30116051

Glutamate protects neuromuscular junctions from deleterious effects of β-amyloid peptide and conversely: An in vitro study in a nerve-muscle coculture.

Combes M, Poindron P, Callizot N.

J Neurosci Res. 2015 Apr ;93(4):633-43. doi : 10.1002/jnr.23524. Epub 2014 Dec 9.

Abstract

Murine models of Alzheimer’s disease with elevated levels of amyloid-β (Aβ) peptide present motor axon defects and neuronal death. Aβ1-42 accumulation is observed in motor neurons and spinal cords of sporadic and familial cases of amyotrophic lateral sclerosis (ALS). Motor neurons are highly susceptible to glutamate, which has a role in ALS neuronal degeneration. The current study investigates the link between Aβ and glutamate in this neurodegenerative process. Primary rat nerve and human muscle cocultures were intoxicated with glutamate or Aβ. Neuromuscular junction (NMJ) mean size and neurite length were evaluated. The role of N-methyl-D-aspartate receptor (NMDAR) was investigated by using MK801. Glutamate and Aβ production were evaluated in culture supernatant. The current study shows that NMJs are highly sensitive to Aβ peptide, that the toxic pathway involves glutamate and NMDAR, and that glutamate and Aβ act in an interlinked manner. Some motor diseases (e.g., ALS), therefore, could be considered from a new point of view related to these balance disturbances.

www.ncbi.nlm.nih.gov/pubmed/25491262

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N6P31

Acute and chronic dopaminergic neurotoxicity of alpha-synuclein oligomers: two distinct mechanisms.

SFN - 2019 - Chicago (USA) - Oct 2019

#PD

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N6P20

Activation of the PERK pathway reduces the proteinopathy associated with neurodegenerative diseases: evidence from in vitro models of AD, PD and ALS.

4th  annual Neuroscience R&D Technologies Conference - Munich (Germany) - Oct 2018

#AD, #PD, #ALS

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N6P13

MPP+ induced dopaminergic neuron death through necroptosis and autophagy.

AD/PD 2015 - Vienna (Austria) - March 2015

#PD

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N6P03

Study of mitochondrial death pathways in different cellular models of Parkinson's disease: effect of 17β-Estradiol.

SFN 2014 - Washington - Nov 2014

#PD

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N6P30

Impairment of lysosomal function contributes to synucleinopathy and neurodegeneration in in vitro models of Parkinson’s disease.

SFN - 2019 - Chicago (USA) - Oct 2019

#PD

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N6P19

Neuroprotective effects of

SNC-1 (Ethnodyne Neuro®), a natural product used in ayurvedic traditional medicine, on in vitro models of Parkinson’s disease.

IAPRD - Lyon (France) - Aug 2018

#PD

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N6P07

Neuroprotective effect of SNC-1 a natural plant extract. Promising treatment for Alzheimer’s and Parkinson’s disease?

Phyt'Arom - Grasse (France) - June 2015

#PD

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N6P22

The acute dopaminergic neurotoxicity of alpha-synuclein oligomers is mediated by microglial cells.

AD/PD 2019 - Lisbon (Portugal) - March 2019

#PD

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N6P18

Acute dopaminergic neurotoxicity of alphasynuclein oligomers is mediated by microglial cells.

IAPRD - Lyon (France) - Aug 2018

#PD

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N6P06

α-synuclein: Cause or consequence of cytopathological lesions observed in in vitro models of Parkinson’s disease.

AD/PD - Geneva (Switzerland) - March 2015

#PD

 
 
 
 

 Collaboration 

Neuro-Sys is open to national, European and international scientific collaboration.

Our R&D department is dedicated to the development and characterisation of models of neurodegenerative diseases.

We investigate the pathological mechanisms involved in these diseases in order to provide relevant models for studying the efficacy and mode of action of therapeutic compounds.

Aside from our intern R&D programs, we are involved in collaborative projects with internationally renowned partners from academia and industry.

Chaperon project (supported by Eurostars program/H2020)

In collaboration with Gain Therapeutics SA (Switzerland) and the Institute for Research in Biomedicine (Switzerland), Neuro-Sys is supported by a European program in the development of novel and innovative models of lysosomal storage diseases (Gaucher’s disease, Krabbe’s disease, Hurler syndrome, GM1 gangliosidosis).This collaborative project is a great opportunity to gain insight into the mechanisms of these rare diseases and to support the development of new therapies.

Proteinopathy in neurodegenerative diseases (collaboration with Sciomics GmbH)

Proteinopathy is a common feature in neurodegenerative diseases. Protein clearance pathways represent promising therapeutic targets for these diseases to alleviate the protein burden.Neuro-Sys and Sciomics GmbH (Germany) have joined forces to study the proteome and the phosphoproteome in preclinical models of Alzheimer’s, Parkinson’s and ALS diseases to investigate the proteomic profiling of these disease models. The aim is to better understand the mechanisms involved in the neurodegenerative process and to provide new solutions for characterising the efficacy and mode of action of neuroprotective compounds.

Sphingolipids in Parkinson’s disease (collaboration with University of Milan) and amyotrophic lateral sclerosis (collaboration with University of Strasbourg)

 

Growing evidence connects complex sphingolipids to trophic signaling in neurodegenerative diseases, such as Parkinson’s disease and amyotrophic lateral sclerosis.

Together with Dr Elena Chiricozzi, from the University of Milan, we are dissecting the effects of complex sphingolipids on different pathologies of Parkinson’s disease (e.g. mitochondrial dysfunction, neuroinflammation).

In a second collaborative project with the Dr Jean-Philippe Loeffler, at the university of Strasbourg, we investigate the neuroprotective pathways linked to glycosphingolipids.

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