Welcome to SynAging SAS

Your R&D partner for in vitro and in vivo phenotypic models in WT, accelerating drug discovery for sporadic neurodegenerative diseases.

News

SynAging has new phone and fax numbers in 2017! Please amend your records accordingly. The old numbers will work until the end of 2017 only!

SynAging will be present at the following meetings in 2017:

European Brain & Behavior Society Meeting, September 8-11, Bilbao, Spain

Neuroscience R&D Technologies Conference, September 28-29, London, UK - Presentation on Sept. 29

Genesis Drug Discovery, October 11-12, Frankfurt, Germany - Presentation on Oct. 11

BIO-Europe 2017, November 6-8, Berlin, Germany

BioFIT 2017, November 28-29, Strassbourg, France, meet us at booth C4

SynAging' past meetings in 2017:

EuroTau Meeting, April 27-28, Lille, France

International Conference on Alzheimer's & Parkinson’s Diseases 2017 - Booth 14a, at the entrance of the exhibition & Posters
March 29 . – April 2., Vienna, Austria

SynAging's past meetings in 2016:

Press & Publications

Structural and functional analyses of pyroglutamate-amyloid-β-specific antibodies as a basis for Alzheimer immunotherapy
www.ncbi.nlm.nih.gov/pubmed/28623233

ProMIS Neurosciences Designates PMN350 its Second Lead Product for Development in Alzheimer’s Disease
promisneurosciences.com/uncategorized/promis-neurosciences-designates-pmn350-second-lead-product-development-alzheimers-disease/

HUMAN TAU OLIGOMERS INDUCE NEURODEGENERATION: TAUOPATHY MODELS FOR TARGET VALIDATION AND DRUG DEVELOPMENT
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HUMAN ALPHA-SYNUCLEIN OLIGOMERS BUT NOT 'SPREADING' FIBRILS INDUCE EARLY COGNITIVE DECLINE IN MICE
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SynAging's human tau oligomer poster at SFN 2016
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SynAging's alpha synuclein oligomer poster at SFN 2016
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SynAging's Alzheimers disease poster at AAIC 2016
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SynAging's Parkinson's disease poster at AAIC 2016
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Excitotoxicity

Excitotoxicity is defined as excessive exposure to glutamate, the main excitatory neurotransmitter in the mammalian CNS. Excitotoxicity has been implicated as a mechanism of brain damage associated with:

  • Stroke
  • Epilepsy
  • Trauma
  • and neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and others

Under normal conditions, glutamate released from the presynaptic neuron activates ionotropic glutamate receptors present on the postsynaptic neuron. This results in the influx of Na+ and Ca2+ ions into the cell, leading to membrane depolarization and generation of action potentials. Overstimulation of glutamate receptors, especially the NMDA subtype, are known to result in neuronal injury and death.

SynAging is offering an in vitro assay inducing neuronal damage and death by glutamate (or NMDA) overstimulation.

This enables the investigation of client’s active substances to prevent or revert excitotoxicity.