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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Parkinson’s Disease

Overview

SynAging provides in vitro and in vivo models to test potential symptomatic and diseases modifying therapeutic candidates for their potential benefit in Parkinson’s disease (PD).

SynAging’s models are based on the neurotoxicity of misfolded-α-synuclein-aggregates:

  • low number soluble oligomers (aSO), or
  • fibrillar preparations α-synuclein (aSF).

Preparations are made in house using a confidential physicochemical protocol, producing highly reproducible results, which is SynAging's specialty. No crossslinkers or helper proteins are used for stabilization. All preparations have long term stability during storage and are validated by quality control, before their application in client projects.

BDNF and EGCG have been validated as positive controls in SynAging’s in vitro model. Test items can be investigated and optimized in our highly reproducible in vitro assays.

SynAging's has two in vivo PD models:
(i) α-synuclein oligomer (aSO) based, showing first cognitive imparement within 15 days in mice, reduction of synaptic markers,  dopaminergic markers, and neuroinflammation. Mice injected with αSO and challenged with amphetamine displayed an anticlockwise circling behaviour, typical for dopaminergic neuron deficit and relevant for movement disorders of Parkinson’s disease. And alternatively:
(ii) sonicated α-synuclein fibril (aSF) based, showing so called 'spreading' within 15 days and cognitive impairment after 90 days.
Both models are induced by a single intra-striatal injection of a small amount of aggregate into the right striatum of WT mice.

Putative PD therapeutics are tested for their capabilities to ameliorate the symptoms, or revert the neurodegeneration in SynAging's models. So far, no public positive control for in vivo models has been identified world wide.

General neurodegeneration models using various stimuli, such as excitotoxicity and oxidative stress can be used to further characterize the effect of test items.

 

Scientific Rational

Please see: Parkinson´s_Disease in Science and Technology