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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Alzheimer´s Dementia

Overview

SynAging provides in vitro and in vivo models to test new symptomatic and neuroprotective treatments for Alzheimer’s dementia (AD). The AD models are based on the effects of a single injection of minute amounts of misfolded protein aggregates on synapses, the innate immune system, and resulting cognitive deficits in rodents.

Soluble oligomers (and fibrils) are prepared by SynAging from:
• amyloid-β peptides (AbO), or
• human tau-proteins (hTO)
in proprietary and confidential protocols resulting in the world-wide highest reproducibility. All preparations are validated by quality control before use in client projects and the performance of the controls is guaranteed by SynAging.

A number of clinical reference compounds and many clients’ compounds have been tested in SynAging’s models. The results of the clinical reference compounds were found to resemble findings from clinical use, suggesting translatability of SynAging's Alzheimer disease model results into the clinic.

Compound candidates can be tested and optimized in:
in vitro assays using acutely isolated primary rodent neurons
in vitro assays using acutely isolated primary astrocytes
in vitro assays using iPS cell derived human neuronal cultures
in vivo assays investigating treatment benefits for various cognitive domains in our various validated cognitive assays in mice

AD treatments can further be tested in general neurodegeneration models using various stimuli, such as excitotoxicity and oxidative stress.

 

 

Scientific Rational

Please see: Alzheimer’s Dementia in Science and Technology