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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Ex Vivo Assays

Sampling:

  • Brain and brain substructures
  • Crude extracts
  • Subcellular fractioning
  • Synaptosomal preparations
  • Membranes and lipid rafts preparations
  • Cerebrospinal fluid
  • Blood, plasma
  • Peripheral tissues

 

Biochemistry / Immunochemistry investigating:

  • Synaptic markers (e.g. SNAP25, PSD 95, synaptophysin, synaptotagmin)
  • Inflammation markers (e.g. IL1β, TNFα, IL6, ...)
  • Cell signaling (e.g. MAPkinase, STAT3, PI3k/Akt, CREB, …)
  • Oxidative stress (e.g. ROS, 4HNE, GSH, …)
  • Amyloid loads (soluble & fibrillar)
  • Lipids and fatty acids

 

SynAging has established the loss of synaptic markers and neuroinflammation in its phenotypic mouse model of Alzheimer’ Disease, which is induced by a single icv injection of its highly reproducible amyloid-β or tau oligomers.

Following behavioral evaluation, SynAging is now offering validated routine quantitative ELISA assays of important pre- and post-synaptic marker proteins:

SNAP25, PSD95, and synaptophysin are reduced significantly in AβO or hTO treated mice and restored by the neuroprotective peptide humanin, validated in multiple independent experiments.To SynAging's knowledge, loss of synaptic markers has not been shown for any other Alzheimer model on the market so far.

Furthermore, induction of TNFα, IL1β and IL6 are reproducibly seen after treatment of primary astrocytes with misfolded protein aggregates. More information is shown in SynAging's Alzheimer in vitro AbO model presentation.The changes of neuroinflammatory markers have also been valuated in the AbO induced mouse in vivo:

 

SynAging’s AbO induce impairment of cell signaling (reduced actin phosphorylation, P-Act, compared to total actin, Act) and synaptic function (reduced presence of: glutamate receptor 2 and 3, GluR2/3) in primary neurons and protection by humanin peptide (HNG).