EVENTS
Actif’s magazine article about Neuro-Sys
"Neuropharmacological and nutraceutical industry"
> Article
25 AVR. 2019 : New publication released
Check out our new Parkinson’s disease paper published in PLOS ONE : Necrosis, apoptosis, necroptosis, three modes of action of dopaminergic neuron neurotoxins.
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.
> Article
July 2019 Press Release
Gain Therapeutics SA Announces Award Notification of a €1.4M Grant Support From Eurostars-2 Together With the Institute for Research in Biomedicine and Neuro-Sys SAS After Having Scored 2nd Among 325 Eligible Applications
> Link to PR
News
JULY 2019 : Gain Therapeutics SA Announces Award Notification of a €1.4M Grant Support From Eurostars-2 Together With the Institute for Research in Biomedicine and Neuro-Sys SAS After Having Scored 2nd Among 325 Eligible Applications
Gain Therapeutics SA Announces Award Notification of a €1.4M Grant Support From Eurostars-2 Together With the Institute for Research in Biomedicine and Neuro-Sys SAS After Having Scored 2nd Among 325 Eligible Applications July 23, 2019 02:30 AM Eastern Daylight Time
LUGANO, (...)
April 2019 : Actif’s magazine article : "Neuropharmacology and nutraceutical industry"
"Founded in 2013 in Gardanne near Aix-en-Provence by a team of pharmacologists specialising in neurodegenerative diseases, Neuro-Sys evaluates the efficacy of compounds and plant extracts... on unique and effective models of cell cultures mimicking these (...)
Janvier 2019 article Biotech Info No91 : "Neuro-Sys : des plantes médicinales pour lutter contre les maladies neurodégénératives."
Neuro-Sys : des plantes médicinales pour lutter contre les maladies neurodégénératives. Son approche repose sur l’usage traditionnel des plantes mais également sur l’étude d’éponges marines pour en extraire les principes actifs efficaces.
Notre recherche a démarré sur les plantes (...)
Dec 11, 2018 Information Release : "Neuro-Sys Highlighted Molecules from Sea Sponges to Fight Neurodegenerative Diseases."
By Neuro-Sys SAS Mgmt / December 11, 2018 / News / www.neuro-sys.com
Sea sponges : a new source of natural products that may contain active substances that can be used to treat neurodegenerative diseases, notably Alzheimer’s disease.
GARDANNE, France – December 11, 2018 – (...)
11 Déc. 2018 Communiqué : "Des molécules issues d’éponges marines pour combattre les maladies neurodégénératives."
Par Neuro-Sys SAS Mgmt / 11 décembre 2018 / News / www.neuro-sys.com
Nouvelle source de produits naturels pouvant contenir des substances actives pouvant être utilisées dans le traitement des maladies neurodégénératives, notamment la maladie d’Alzheimer : les éponges marines. (...)
30/10/2018 Article La Provence : "Les plantes pour ralentir les maladies neurodégénératives."
Les plantes pour ralentir les maladies neurodégénératives.
Les recherches de la start-up gardannaise Neuro-Sys se concrétisent.
Charcot, Alzheimer, Parkinson, les maladies neurodégénératives sont nombreuses et d’une dureté effroyable. A Gardanne, la start-up Neuro-Sys a déjà déposé (...)
Posters
AAIC 2019
14-18 July 2019, Los Angeles (USA)
Tau Site-specific hyperphosphorylation by Aβ oligomers and glutamate in a primary culture of cortical neurons.
PNS 2019
24-26 June 2019, Genoa (Italy)
The Chemotherapy-induced peripheral neuropathy involves specific neural or Schwann cell targets. The case of Cisplatin, Taxol and Vincristine.
METASUD 2019 - NSP06
12-13 June 2019, Toulon (France)
Neuroprotective activity of NSP06 : an ecofriendly plant extract from Verbena officinalis
NEUROFRANCE 2019 - ALS
24-22 May 2019, Marseille (France)
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.
AD/PD 2019 - PD
25-31 March 2019, Lisbon (Portugal)
Acute dopaminergic neurotoxicity of alpha-synuclein oligomers is mediated by microglial cells.
AD/PD 2019 - AD
25-31 March 2019, Lisbon (Portugal)
Effect of DAPK1 inhibition on the site-specific hyperphosphorylation of Tau in two in vitro models of Alzheimer’s disease, injured by glutamate or Aβ oligomers.
MNDA 2018 - ALS
7-9 December 2018, Glasgow (UK)
Translocation of TDP-43 and FUS in cortical neurons and spinal motor neurons after glutamatergic stress or in presence of the neurotoxic peptide Aβ1-42.
ISCNP 2018 - AD (NSP01)
25-29 November 2018, Athens (Greece)
From traditional use to standardized neuroprotective green-extract of Huperzia serrata.
MNM 2018 - ER STRESS
04-05 October 2018, Munich (Germany)
Activation of the PERK pathway reduces the proteinopathy associated with neurodegenerative diseases : evidence from in vitro models of AD, PD and ALS.
IAPRD 2018 - PD
19-22 August 2018, Lyon (France)
Acute dopaminergic neurotoxicity of alphasynuclein oligomers is mediated by microglial cells.
IAPRD 2018 - PD (SNC1)
19-22 August 2018, Lyon (France)
Neuroprotective effects of SNC-1 (Ethnodyne Neuro®), a natural product used in ayurvedic traditional medicine, on in vitro models of Parkinson’s disease.
SOCIETE DES NEUROSCIENCES - AD
7-8 June 2018, Strasbourg (France)
ER-stress regulation and effect of Guanabenz in primary cortical neurons injured with Aβ1-42 peptide, an in vitro model of Alzheimer’s disease.
AAT-AD/PD 2018 - AD
15-18 March 2018, Torino (Italy)
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.
MNM 2017 - PD (SNC1)
28-29 September 2017, London (UK)
SNC-1 a natural food supplement, a promising candidate for the treatment of Parkinson’s Disease.
MNM 2017 - BBB
28-29 September 2017, London (UK)
Effects of circulating and neuronal amyloid peptide oligomers on BBB integrity : consequences for the disease.
AAIC 2017 - BBB
16-20 July 2017, London (UK)
Effects of circulating and neuronal amyloid peptide oligomers on the BBB integrity : consequences on the neurodegeneration process.
AD/PD 2017 - PD
29 March - 02 April 2017, Vienna (Austria)
MPP+ induced dopaminergic neuron death through necroptosis and autophagy.
AD/PD 2017 - ALS
29 March - 02 April 2017, Vienna (Austria)
Amyloid peptide and cytoplasmic TDP-43 accumulation in pathogenesis of ALS : an in vitro study.
MNM 2016 - AD/BBB
29-30 September 2016, London (UK)
A novel triple cell co-culture model for mimicking the BBB into normal or pathological situations.
AAIC 2016 - AD
22-28 July 2016, Toronto (Canada)
Mode of action study of NSP01-E, a potential treatment for Alzheimer’s disease, in protection against amyloid β peptide (Aβ) injury.
MYOLOGY 2016 - ALS
14-18 March 2016, Lyon (France)
Pathological role of amyloid peptide in neuromuscular disease, glutamate and glucose involvement.
JSFM 2015 - ALS
23-25 November 2015, Lyon (France)
Deleterious effects of amyloid beta peptide in the neuromuscular junction : consequences in ALS disease.
PHYT’AROM 2015 - SNC-1
5-7 June 2015, Grasse (France)
Neuroprotective effect of SNC-1 a natural plant extract. Promising treatment for Alzheimer’s and Parkinson’s disease ?
AD/PD 2015 - PD
18-22 March 2015, Nice (France)
α-synuclein : cause or consequence of cytopathological lesions observed in in vitro models of Parkinson’s disease.
AD/PD 2015 - AD
18-22 March 2015, Nice (France)
Neurodegeneration induced by Aβ oligomeric fractions : role of NMDA receptors and mGluR5.
ARUK CONF. 2015 - AD
10-11 March 2015, London (UK)
NSP01-E01 and NSP01-C01 : new preparations able to protect from beta-amyloid peptide (Aβ) injuries. Potential treatments for Alzheimer’s disease.
SFN 2014 - PD
15-19 November 2014, Washington (USA)
Study of mitochondrial death pathways in different cellular models of Parkinson’s disease : effect of 17β-Estradiol.
SFN 2014 - AD
15-19 November 2014, Washington (USA)
Beta-estradiol protects cortical neurons from beta-amyloid oligomers toxicity through mediations of the Ras/raf and PI3K pathways.
ICNMD 2014 - ALS
5-10 July 2014, Nice (France)
Role of β-Amyloid (Aβ) Oligomeric fractions in ALS disease.
Publications
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.
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.
Necrosis, apoptosis, necroptosis, three modes of action of dopaminergic neuron neurotoxins
Noelle Callizot , Maud Combes, Alexandre Henriques, Philippe Poindron
Published : April 25, 2019https://doi.org/10.1371/journal.pone.0215277.
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.
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