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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Alzheimer’s Dementia

Alzheimer’s disease and its symptoms in patients are well described on the web pages of the Alzheimer’s Society.

In summary AD:

  • Is the most prevalent form of (age-related) dementia
  • Cannot be cured
  • Is currently only transient and moderately improved by symptomatic treatment
  • Has epidemic-like proportions with close to 26 millions patients diagnosed worldwide
    (projections: more than 100 millions in 2050)
  • Is a major challenge for society and public health systems, as late stage patients need 24/7 monitoring

The molecular causes of the disease are still not fully understood. However, the amyloid precursor protein (APP) on chromosome 21 is involved in AD, because:

  • Trisomy 21 patients always get AD like symptoms early in life
  • Rare (<1% of AD patients) APP mutations result in early onset AD
  • Oligomers of Aβ peptides are neurotoxic, inducing cognitive defects

The amyloid hypothesis has been around for more than 20 years, predicting that Aβ peptides and their macromolecular aggregates called “plaques” cause the disease. However, Aβ peptide monomers are not toxic, but likely beneficial for brain function. Plaque aggregates are neither toxic nor well correlated with dementia as shown e.g. in the continuing longitudinal Nun study where strong AD plaque pathology in non-demented people was explained by “brain reserves” (www.healthstudies.umn.edu/nunstudy/articles).

Recently it was found that low molecular weight soluble oligomers of Aβ are formed in AD brains and that these oligomers are highly toxic to important brain targets involved in cognition. Furthermore, Aβ oligomers are thought to induce holes in the cell membrane (www.mdpi.com/1422-0067/13/6/7303/pdf). A review on Aβ oligomer toxicity can be found here: http://www.nature.com/neuro/journal/v15/n3/full/nn.3028.html.

SynAging scientists have contributed significantly to the field of Aβ oligomer toxicity (http://www.neurobiologyofaging.org/article/S0197-4580(07)00115-7/abstract) and established very reliable, fast and cost-effective models. These models are based on proprietary Aβ peptide oligomer preparations of various Aβ peptides (link to table). These models have been established in 2010 and since then are used on a continuous base by many international clients.