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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Neurodegeneration (general)

Neurodegeneration is the general term for the progressive loss of function and integrity of neuronal networks, including death of neurons associated with neuroinflammatory processes. Neurodegeneration can be found in many different levels of neuronal circuitry ranging from molecular to systemic. Many neurodegenerative diseases including Parkinson’s, Alzheimer’s, and Huntington’s occur as a result of specific disease processes destabilizing neuronal network integrity that have been associated to accumulation of misfolded proteins or peptides. Many similarities appear in the progression of these diseases on a cellular and molecular level. These biochemical insults to neurons are mimicked in our neurodegenerative disease models. There are many parallels between different neurodegenerative disorders including protein misfolding and aggregation, oxidative stress, and overstimulation by excitatory neurotransmitters. As research progresses, the presence of soluble and diffusible oligomeric structures may relate these diseases to one another on a molecular and sub-cellular level.

Discovering these similarities offers hope for therapeutic advances that could ameliorate many diseases simultaneously.

Please choose one of the models from the menu for further information.