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' 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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SynAging Provides Innovative Models for Neurodegenerative Diseases

Neurological diseases are among the most common threats to human health and difficult to treat. Millions of people are affected, especially in aging societies. Today there are no cures for neurological diseases and effective drug therapies are very much needed. For decades drug development programs addressing common diseases of the central nervous system (CNS) show particularly high failure rates and little progress. Clearly, clinicians and researchers require much better in vitro and in vivo models to identify and develop new, effective and safe drugs.

In recent years, advances in neurobiology helped to understand the pivotal role of soluble prion-like misfolded protein aggregates in the formation of neurodegenerative diseases. SynAging builds on these insights and has proprietary procedures to create these aggregates with highest reproducibility. Oligomers are used in vitro and in vivo to induce neurodegeneration acutely and provide drug developers with fast access to phenotypic models mimicking the corresponding neurodegenerative disease.

SynAging focuses on disease-inducing misfolded protein aggregates, which are involved in all stages of age-related neurodegenerative diseases.

See Science and Technology.

 

SynAging is a contract research organization (CRO) which provides:

  • Disease relevance to facilitate translation into clinical development
  • High reproducibility and reliability
  • Better results faster
  • Cost-effective services

SynAging’s services include proprietary models e.g. for Alzheimer’s Dementia (AD) and Parkinson's disease (PD) and are continuously expanded to cover other neurodegenerative indications by providing new and better models.