Welcome to SynAging SAS

Your R&D partner for in vitro and in vivo phenotypic models in wild type, 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:

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

Genesis Drug Discovery, October 11-12, Frankfurt Main, 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:

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

20 Years of alpha-synuclein in Parkinsion's disease and related synucleopathies Meeting in Athens, September 7-10, 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

SynAging's Poster won the 'Best Poster Award' here during the '20 Years of alpha-synuclein in Parkinsion's disease and related synucleopathies' meeting in Athens, September 7-10, 2017 entitled:
PATHOLOGICAL ALPHA-SYNUCLEIN PREPARATIONS INDUCE COGNITIVE IMPAIRMENT AND NEURODEGENERATION
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Poster EBBS Meeting 2017: PRION-LIKE SOLUBLE MISFOLDED PROTEIN OLIGOMERS INDUCE NEURODEGENERATION: RELEVANCE FOR PARKINSON’S AND ALZHEIMER’S DISEASE MODELS
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Dietary arachidonic acid increases deleterious effects of amyloid-β oligomers on learning abilities and expression of AMPA receptors: putative role of the ACSL4-cPLA2 balance;  Link

Structural and functional analyses of pyroglutamate-amyloid-β-specific antibodies as a basis for Alzheimer immunotherapy
Link

ProMIS Neurosciences Designates PMN350 its Second Lead Product for Development in Alzheimer’s Disease
Link

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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Scientific Basis

SynAging puts disease-inducing misfolded-protein-oligomers involved in the earliest stages of age-related neurodegenerative diseases in the center of the drug discovery processes.

A number of neurodegenerative diseases and some systemic diseases are caused by misfolded-protein-aggregates. In the literature (including SynAging’s publications), there is accumulating evidence for a critical role of oligomers of low molecular weight (soluble and diffusible assemblies) in synaptic and neuronal degeneration, and more generally in cell toxicity. This toxicity is already occurring in the early stages of amyloid-associated diseases, but sometime only observed at a later advanced stage.

SynAging has mastered the reproducible preparation and use of such oligomerized and polymerized protein preparations and the evaluation of their toxic effects in vitro, in vivo and in ex vivo biochemical studies of marker proteins.

  • The main advantage of SynAging’s technology is the reproducible preparation of low number oligomers at high concentrations from various amyloidogenic proteins or peptides inducing consistent effects in vitro and in vivo.
  • The use of the same oligomer preparation enables a fast and reliable transition from in vitro to in vivo model, increasing translatability and consistency of results.
  • SynAging’s technology allows the easy combination of protein oligomer induced stress plus age dependent stress that is one of the major virtues* for a valid animal model and consequently the discovery of efficient therapeutics for neurodegenerative diseases.

* Review of Ramanan & Sykin “Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer's disease, Parkinson's disease, and related disorders.”, http://www.ncbi.nlm.nih.gov/pubmed/24093081