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
Download PDF
 

Poster EBBS Meeting 2017: PRION-LIKE SOLUBLE MISFOLDED PROTEIN OLIGOMERS INDUCE NEURODEGENERATION: RELEVANCE FOR PARKINSON’S AND ALZHEIMER’S DISEASE MODELS
Download PDF

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
Download PDF

HUMAN ALPHA-SYNUCLEIN OLIGOMERS BUT NOT 'SPREADING' FIBRILS INDUCE EARLY COGNITIVE DECLINE IN MICE
Download PDF

SynAging's human tau oligomer poster at SFN 2016
Download PDF

SynAging's alpha synuclein oligomer poster at SFN 2016
Download PDF

SynAging's Alzheimers disease poster at AAIC 2016
Download PDF

SynAging's Parkinson's disease poster at AAIC 2016
Download PDF

 

Disease Models

Neurodegenerative diseases are our first priority, with a special emphasis on Alzheimer’s Dementia (AD) associated with beta-amyloid and tau oligomers and fibrils, Parkinson’s Disease (PD) with α-synuclein oligomers and fibrils, Creutzfeldt–Jakob Disease (CJD) with abnormal prion proteins, and Huntington’s Disease (HD) with misfolding and aggregation of “huntingtin” proteins. SynAging’s scientists have contributed towards the understanding of which aggregates are toxic and what could be the mechanism of neurodegeneration.

Successful drug development requires the use of relevant disease models. SynAging endeavors to offer in vitro and in vivo models for all these diseases, which most accurately represent the biochemical cause of the disease under investigation. In this context, SynAging scientists are constantly monitoring the scientific literature adapting new scientific insights into disease mechanisms.

SynAging’s in vitro models are often used for hit validation following biochemical screens, investigating tens to hundreds of potential lead candidates for activity in relevant phenotypic disease models and giving a first indication towards their potency.

SynAging’s in vivo models are further used for lead selection and optimization, taking more advanced drug candidates into animal models that investigate multiple disease relevant behaviors and read-outs.

SynAging is specialized on protein aggregate caused human disease. Such diseases are often called 'amyloidosis' and recently also proteopathic or proteinopathic diseases, and comprise a number of incurable degenerative diseases. The protein aggregates are not degradable in the human body and accumulate often causing cell malfunctioning or death.

Neurodegenerative diseases are SynAging’s main focus, with unique capabilities in Alzheimer’s Dementia (AD) and Parkinson's disease (PD). SynAging’s scientists are constantly expaning our service portfolio and contributing towards the understanding of these diseases.

For further information please choose the disease of interest from the menu on the left.