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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Ex vivo Analysis of α-Synuclein-Aggregate-Induced Parkinson’s Disease Models

Misfolded α-synuclein aggregate induced mouse models have been investigated for:

  • Synaptic Marker Loss
  • Dopaminergic Marker Loss
  • 'Spreading' in Mouse Brain
  • Neuroinflammatory Markers

Synaptic marker loss:                                                           Dopaminergic marker loss:

                                         

 'Spreading' in aSF induced mouse brain:

 

 Neuroinflammatory marker induction:                                  Iba1 imaging of activated microglia: