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:
Society for Neuroscience (SfN) 2016 - Posters
November 12. - 16, San Diego, USA
BIO-Europe 2016, Partnering
November 7. – 9, Cologne, Germany
3rd International Parkinson´s Disease Symposium 2016 - Booth, Symposium & Posters
October 6 - 8, Luxembourg
10th Forum of Neuroscience - Poster
July 2.-6. 2016, Copenhagen, Denmark
Alzheimer's Association International Conference 2016 - Booth 825 & Posters
July 24. – 28. 2016, Toronto, Canada
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 Download PDF
Poster EBBS Meeting 2017: PRION-LIKE SOLUBLE MISFOLDED PROTEIN OLIGOMERS INDUCE NEURODEGENERATION: RELEVANCE FOR PARKINSON’S AND ALZHEIMER’S DISEASE MODELS Download PDF
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 Download PDF
HUMAN ALPHA-SYNUCLEIN OLIGOMERS BUT NOT 'SPREADING' FIBRILS INDUCE EARLY COGNITIVE DECLINE IN MICE Download PDF
SynAging's human tau oligomer poster at SFN 2016 Download PDF
SynAging's alpha synuclein oligomer poster at SFN 2016 Download PDF
SynAging's Alzheimers disease poster at AAIC 2016 Download PDF
SynAging's Parkinson's disease poster at AAIC 2016 Download PDF
True alignment of preclinical and clinical research to enhance success in CNS drug development: a review of the current evidence.
Goetghebeur PJ, Swartz JE www.ncbi.nlm.nih.gov/pubmed/27147593
Alzheimer therapy with an antibody against N-terminal Abeta 4-X and pyroglutamate Abeta 3-X Download PDF, 1.3 MB
SynAging announces extension of its collaboration with Europe's largest biopharmaceutical company Download PDF
First Commercial in vitro Test System for Human Neuroprotection in Proteopathic Diseases such as Alzheimer’s and Parkinson’s Download PDF
SynAging Expands its Capabilities: Building a New Animal Facility and Hiring a Head of Pharmacology Download PDF, 150 KB
Prions are misfolded protein species known to cause neurodegeneration in vivo called transmissible spongiform encephalopathies (TSEs), a group of progressive encephalopathies that affect the brain and nervous system of animals and humans. Mental and physical abilities deteriorate and holes appear in the cortex giving the brain tissue a sponge-like-appearance. The disorders cause a steadily worsening impairment of brain function:
Examples include classic Creutzfeldt–Jakob disease, the new variant Creutzfeldt–Jakob disease (nvCJD, a human disorder thought to be induced by the consumption of bovine meat of animals with spongiform encephalopathy - BSE), Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia and Kuru.
SynAging is using prion-protein-derived oligomer preparations on primary neuronal cultures to model prion disease and induce neurodegeneration and neuronal death.
This enables mechanistic studies of prion-induced neurodegeneration in vitro.
Clients can study their active substances for the ability to prevent or revert prion-derived neurotoxicity in SynAgings assays.
This model of PrP-derived low number oligomers is supported by key publications:
Sponne I, Fifre A, Koziel V, Kriem B, Oster T, Olivier JL, Pillot T. Oligodendrocytes are susceptible to apoptotic cell death induced by prion protein-derived peptides. Glia. 2004 Jul;47(1):1-8.
Sponne I, Fifre A, Koziel V, Kriem B, Oster T, Pillot T. Humanin rescues cortical neurons from prion-peptide-induced apoptosis. Mol. Cell. Neurosci. 2004 Jan;25(1):95-102.
Pillot T, Drouet B, Pinçon-Raymond M, Vandekerckhove J, Rosseneu M, Chambaz J. A nonfibrillar form of the fusogenic prion protein fragment [118-135] induces apoptotic cell death in rat cortical neurons. J. Neurochem. 2000 Dec;75(6):2298-308.
Pillot T, Lins L, Goethals M, Vanloo B, Baert J, Vandekerckhove J, Rosseneu M, Brasseur R. The 118-135 peptide of the human prion protein forms amyloid fibrils and induces liposome fusion. J. Mol. Biol. 1997 Dec 5;274(3):381-93.