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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In vitro Rodent Models of Parkinson’s Disease

Overview

 

  • Mouse primary striatal neurons are the most sensitive neurons to the oligomers of mouse or human α-synuclein (αSO), more than cortical, cerebellar, or hippocampal neurons.
  • 400 nM αSO kill ̴ 40% of mouse primary striatal neurons within 72 h.
  • Typical in vitro assay results for antibodies or small molecules are shown below (Figure 1)
  • Various fibrillar forms of α-synuclein, made by multiple academic labs, show similar dose-dependent neurotoxicity on primary striatal neurons after 72 h. However, SynAging’s αSO are the most toxic conformation (Figure 2)
  • BDNF (50 nM) is a suitable positive control preventing αSO neurotoxicity (Figure 3).
  • SynAging's high reproducibility for producing misfolded α-synuclein aggregates with the same effects is shown at the end of the page.

Product Sheet “In Vitro Neuroprotection Screen for Parkinson’s Disease” Download PDF, 890 KB

 

Neuronal Death in % of all Neurons

Cell viability

Assay setup:

  • primary mouse striatal neurons are seeded in 48-well plates
  • at day 11, medium is supplemented with 400nM αSO preparation
  • neuronal viability is determined 72h later with the MTT or ATP-Light assay
  • test items can be added before, together with, or after the challenge with αSO
  • standard plate layout is in triplicates, including vehicle control, negative control (αSO), positive control (αSO and BDNF), and compounds controls (no αSO)
  • In one 48 well plate (design below):
    6 compounds can be tested at a single concentration,
    2 compounds can be tested at three concentrations, 
    or one compounds in dose response mode, six concentrations
  • αSO-treated neurons show (Figure 4):
    • severe cell shrinkage
    • destruction of the neuronal network
    • phenotype different from AβO
    • slower damage than AβO
  • αSO preparation is highly reproducible in the resulting neurodegenerative properties (Figure 5)

 

Product Sheet “In Vitro Neuroprotection Screen for Parkinson’s Disease”, Download PDF, 2.2 MB

 

one 48 well plate

 

compounds controls