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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n vitro Rodent Models of Alzheimer's Disease

Primary neuronal cultures from rodents or cell lines are used to mimic Alzheimer's dementia in vitro. SynAging's proprietary amyloid-β oligomer (AβO) preparations are used to induce neurodegeneration on day 0. Client’s drug candidates can be applied on day -x to prevent, or on day 0 to reverse neurodegeneration. Various read-outs (see below) have been successfully employed. The MTT and ATP-lite assay are the primary read-out for neuronal survival after 24 - 72h incubation in this model, and further assays investigating other aspects of AβO toxicity and its prevention have been successfully applied:

Further read-outs have been adapted in this model:

  • Gene expression changes (rt qPCR)
  • Protein phosphorylation
  • ELISA quantification of synaptic markers (e.g. SNAP25, PSD95, synaptophysin, synaptotagmin)
  • Oxidative stress
  • Inflammation
  • Cell signaling
  • Gene silencing (RNAi)
  • Morphometric studies
  • Membrane remodeling
  • And functional target investigations

 

MAP-2 labeling of rodent primary neurons

Cell cultures used:

  • Primary neuronal culture from mouse and rat
    • Hippocampal neurons
    • Cortical neurons
    • Striatal neurons
    • Primary Astrocytes
    • Mixed cultures of neurons and glia cells
  • Neuronal and glial cell lines (e.g. SY5Y, HT22, N2a,…)

 

The price of investigating one to three compounds at multiple concentrations in the basic in vitro model starts from a few thousand Euro, please ask for a quote. Please contact us to discuss your interests and requirements for this model.

 

Product Sheet “In vitro Screen on Primary Rodent Neurons”, Download PDF

 

Alzheimer's Disease and Neuroprotective Model in Microfluidic Devise

Primary neurons (here from mouse cortex) have been grown in a microfluidic chamber as described in Taylor et al. (Nature Methods, 2005, 2:599–605) to separate the soma and dendrites from axons and perform mechanistic investigations of disease and rescue. Both compartments can be treated independently with test item, without interchanging medium. Aβ Oligomers (AβO) are introduced exclusively to the axonal compartment and result in synaptic and axonal degeneration. Within 24h the neurodegeneration spreads to the soma, inducing apoptosis, which can be quantified by DAPI staining:

Applications:

  • Insights in drug candidate mode-of-action
  • Investigate compound activity on AβO interaction with axons and retrograde messaging to soma and nucleus
  • Giving insights regarding target location and engagement
  • Time course studies of quantifiable phenotypes
  • Pre-incubation of axonal or soma-dendritic compartment with drug candidate before AβO induction, to investigate neuronal protection rather than direct AβO competition

Product Sheet “Mode of Action Study on Primary Rodent Neurons in Microfluidic Devise”, Download PDF

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