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! The old numbers will stop working soon!

SynAging will be present at the following meetings in 2017:

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

SynAging' past 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

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:

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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In vivo Models of α-Synuclein Aggregate Induced Parkinson´s Disease

So far, commercial models of Parkinson’s disease are based on toxin-induced (e.g. MPTP, rotenone) degeneration of dopaminergic neurons, inducing physiological and functional changes similar to Parkinson’s disease. However, even in genetic background without endogenous α-synuclein expression.

SynAging's in vivo PD model presented below is aimed to resemble the natural sporadic onset of the disease by using misfolded α-synuclein aggregates that have recently been accepted in the scientific community as key factors in the etiology of Parkinson’s disease.

WT 15 weeks old C57BL/6 mice are injected once intra-striatal with human α-synuclein oligomers (aSO), or sonicated human α-synuclein fibrils (aSF) at day 0. Cognitive deficits are observed in the Novel Object Recognition (NOR) assay and Spatial Recognition Test (SRT), but not in the Y-maze.

The 'Discrimination Index' given below describes the preference of mice for a novel object / novel environment, which is absent in cognitively impared mice.

SynAging's results further show that mice injected with aSF develop an α-synuclein pathology (seeding and spreading) within
15 days and expanding up to three month. No correlation of α-synuclein pathology and NOR deficits seems to exist.

 

On the other hand, our results clearly show that mice injected with aSO (single intra-striatal injection) do not develop α-synuclein pathology, even after 3 months. SynAging established that NOR deficits in these mice are correlated with decrease of synaptic markers in the hippocampus by ELISA quantification of synaptophysin, PSD95 and SNAP25, at the same time neuroinflammatory markers are upregulated and microglia are activated.
SynAging has established that mice injected with αSO and challenged with amphetamine displayed an anticlockwise circling behavior, typical for dopaminergic neuron deficit and relevant for Parkinson’s disease. No significant movement degeneration was observed by Rotarod, grip test, string tests and adhesive removal test up to 3 months.

SynAging is investigating this novel PD model further.

SynAging is offering drug candidate trials in the well validated aSO or aSFO induced model!

 

Please contact us to discuss your interests and requirements for this model.

Product Sheet In vivo PD Screen”, Download PDF, 1,5 MB