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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Prion Toxicity

Prions are misfolded protein species known to cause neurodegeneration in vivo called transmissible spongiform encephalopathies (TSEs), a group of progressive encephalopathies that affect the brain and nervous system of animals and humans. Mental and physical abilities deteriorate and holes appear in the cortex giving the brain tissue a sponge-like-appearance. The disorders cause a steadily worsening impairment of brain function:

  • Cognitive decline
  • Behavioral changes
  • Movement disorders

Examples include classic Creutzfeldt–Jakob disease, the new variant Creutzfeldt–Jakob disease (nvCJD, a human disorder thought to be induced by the consumption of bovine meat of animals with spongiform encephalopathy - BSE), Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia and Kuru.

SynAging is using prion-protein-derived oligomer preparations on primary neuronal cultures to model prion disease and induce neurodegeneration and neuronal death.

This enables mechanistic studies of prion-induced neurodegeneration in vitro.

Clients can study their active substances for the ability to prevent or revert prion-derived neurotoxicity in SynAgings assays.

This model of PrP-derived low number oligomers is supported by key publications:

Sponne I, Fifre A, Koziel V, Kriem B, Oster T, Olivier JL, Pillot T. Oligodendrocytes are susceptible to apoptotic cell death induced by prion protein-derived peptides. Glia. 2004 Jul;47(1):1-8.

Sponne I, Fifre A, Koziel V, Kriem B, Oster T, Pillot T. Humanin rescues cortical neurons from prion-peptide-induced apoptosis. Mol. Cell. Neurosci. 2004 Jan;25(1):95-102.

Pillot T, Drouet B, Pinçon-Raymond M, Vandekerckhove J, Rosseneu M, Chambaz J. A nonfibrillar form of the fusogenic prion protein fragment [118-135] induces apoptotic cell death in rat cortical neurons. J. Neurochem. 2000 Dec;75(6):2298-308.

Pillot T, Lins L, Goethals M, Vanloo B, Baert J, Vandekerckhove J, Rosseneu M, Brasseur R. The 118-135 peptide of the human prion protein forms amyloid fibrils and induces liposome fusion. J. Mol. Biol. 1997 Dec 5;274(3):381-93.