Scientific events

NEUROFIT is a pre-clinical CRO dedicated to the evaluation of treatments for CNS and PNS disorders. Therefore, our team of experts elaborates new models to address the challenges of the current drug development and to attend best the needs and wishes of our customers. ( find out more : THERAPEUTIC AREA / TESTS )


  • Neurex: Neuroscience Upper Rhine network
    October 3RD 2017
    Strasbourg, France




    Because we believe research is also made of human interactions, NEUROFIT team is happy to support NEUREX in the context of the project «Trinational Neuro-Campus». This event is proposed in collaboration with PRESTWICK CHEMICAL company.


    ■ October 3, 2017 (02:00 PM - 04:30 PM)
    in Neurofit place

    NEUREX is one of the most important European networks in the field of neuroscience, be it basic, fundamental or applied. Structured in 2001, it federates a hundred and ten laboratories and more than a thousand researchers within the universities of Strasbourg (France), Basel (Switzerland) and Freiburg im Breisgau (Germany).

  • 47th SFN Annual Meeting
    11 - 15 November 2017
    Washington, DC, USA




    An unmissable moment !!! Neurofit team looks forward to meet its worldwide partners during the SFN 2017 meeting (booth 1205) to exchange about past, present and futur projects.


    ■ November 13, 2017 (08:00 AM - 09:00 AM)


    Poster presenter:
    Dr. Stephanie Wagner
    (Neurobiology Group Leader)

    Poster 304.01 / X23: Cognitive impairment induced by systemic inflammation in mice

    E. Andriambeloson · B .Huyard · E. Poiraud · F. Lauga · C. Neveu · S. Wagner

    Neurofit SAS, In vivo, ILLKIRCH, France.

    Systemic inflammation is believed to play a role in ageing as well as in various dementia-related neurological disorders. Indeed, several lines of evidence indicate positive association between systemic inflammation and cognition and other aspects of behaviour in the elderly and demented. The present study was conducted to investigate the impact of systemic inflammation on cognitive function in mice. To this end, a single intraperitoneal administration of a non-septic dose of lipopolysaccharide (LPS) (0.25 mg/kg) was undertaken and the time course of cognitive decline was assessed. Reduced spontaneous alternation of mice in a T-maze was used as a measure of cognitive deficit. Results showed that 1 week after the injection of LPS, a dramatic reduction in the alternation of mice in the T-maze was observed which suggests a cognitive deficit in LPS-treated mice. Although the cognitive deficit persisted for up to 3 weeks following LPS injection there was no change of the general health of mice. Furthermore, the locomotor behavior of LPS-mice as assessed by spontaneous free exploration in the open-field was comparable to that of naive mice. The treatment of LPS- treated mice with Memantine, a drug approved for cognitive enhancement in the elderly, fully restored their cognitive performance. Similar pattern of result was obtained with donepezil, another approved cognitive enhancer drug. Moreover, LPS-induced cognitive deficit was fully prevented by treatment of mice with anti-inflammatory drugs such as dexamethasone or ibuprofen, which confirmed the inflammatory-driven mechanism of LPS-induced cognitive impairment. This mechanism was supported by the increased levels of inflammatory mediators (TNF- and IL1-) in the hippocampus. Interestingly, cognitive relapse was observed after discontinuation of the anti-inflammatory therapy, which indicates the presence of an underlying chronic and persistent inflammation process. Taken together, these above results suggest that low grade systemic inflammation is capable of mediating sustained cognitive impairment in mice.

    ■ November 13, 2017 (03:00 PM - 04:00 PM)


    Poster presenter:
    Dr. Stephanie Wagner
    (Neurobiology Group Leader)

    Poster 396.11 / DD34: Acute and sustained excitoxicity differentially influence riluzole’s neuroprotective effect

    S. Wagner · E. Andriambeloson · C. Neveu

    Neurofit SAS, In vivo, ILLKIRCH, France.

    Excitotoxicity is caused by overstimulation of glutamate receptors. This pathological process that results from excessive release glutamate leads to neuronal injury or death in various neurological disease conditions. An acute elevation of glutamate is thought to induce neuronal injury in conditions such as stroke, epilepsy and brain trauma injury. More chronic and sustained exposure to milder elevations of glutamate is believed to mediate excitotoxicity in neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS). The aim of the present study was to compare the excitotoxic effect of acute (10 – 60 min) and sustained (24 h) exposure to glutamate by cultures of cortical neurons. The neuroprotective effect of riluzole (the unique FDA-approved drug ALS drug) was comparatively assessed under the two glutamate exposure conditions. Two biochemical measurements were used to evaluate glutamate-induced neuronal damage 1 day after the initiation of excitotoxicity: i) measure of the increase in the amount of lactate dehydrogenase (LDH) released in the cell culture supernatant and ii) measure of the decrease in the ATP level in the cell culture. Acute exposure of cortical neurons to glutamate (3, 10, 20 and 75 µM) produced a concentration-dependent increase in extracellular LDH (up to 2-fold increase as compared to the control). When the exposure was extended to 24 h, the amount of extracellular LDH became even more elevated (up to 4-fold increase). Whilst riluzole treatment did not prevent the increase in LDH observed after acute glutamate exposure, it fully abolished the further increase in LDH induced by the sustained exposure. These results suggest that sustained exposure to glutamate induces an additional mechanism of death which is sensitive to riluzole, unlike the one caused by acute exposure. A similar pattern of results was observed when using the decrease of ATP level as a measure of neuronal damage. The above results suggest that acute and sustained exposure to glutamate induce differential mechanisms of neuronal death and this finding is supportive of the beneficial effect of riluzole in neurodegenerative diseases such as amyotrophic lateral sclerosis where more chronic exposure to glutamate is hypothesized.

    Dr. Stephanie Wagner will be present in front of the posters during the whole sessions (respectively 08:00 AM – 12:00 PM and 12:00 PM – 05:00 PM) to answer your questions, at your convenience.

  • 6th BIOFIT EXHIBITION
    28 - 29 November 2017
    Strasbourg, France




    A preferred opportunity to exchange !!! Neurofit team would be happy to meet you at BIOFIT 2017 during organized partnering sessions.

    For registered companies, please use the automated partnering system to schedule a face to face meeting with Dr. Andriambeloson, Head of Research:


    Otherwise, you can contact us directly !
    We are looking forward to hearing from you.

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