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
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

 

Parkinson’s Disease

Parkinson's disease (PD) is a neurodegenerative disorder starting with motor symptoms, resulting from the death of dopamine-generating neurons in the substantia nigra. The neurodegeneration has been recently attributed to misfolded α-synuclein aggregates. Early in the course of the disease, the most obvious symptoms are shaking, rigidity, slowness of movement and gait difficulty. Later, cognitive deficits become more obvious. Parkinson's disease affects people over the age of 50.

The pathology of the disease is characterized by the accumulation of α-synuclein in Lewy bodies in neurons, and by dopamine reduction produced in the substantia nigra. The anatomical distribution of the Lewy bodies appears to be related to the degree of the clinical symptoms of the individual.

Scientific literature has recently documented that misfolded α-synuclein, e.g. in a fibrillar form, can induce 'spreading' of α-synuclein aggregation in rodents. This implies that the presence of misfolded α-synuclein can induce further misfolding in adjacent neurons. The mechanism is internationally agreed to be mediated by misfolded protein, e.g. fibrillar forms, predominately consisting of β-sheet structures, via 'protein structure induction' in unfolded and non-toxic monomers to spread the disease in a prion-like mechanism. Together with e.g. Alzheimer’s disease, Huntington’s disease, PD is now called a proteopathic neurodegenerative disease.

 

References:

“Structural and functional characterization of two alpha-synuclein strains”; Luc Bousset, Laura Pieri, Gemma Ruiz-Arlandis, Julia Gath, Poul Henning Jensen, Birgit Habenstein, Karine Madiona, Vincent Olieric, AnjaBöckmann, Beat H. Meie and Ronald Melki; 2013; Nat. Commun. 4:2575 doi: 10.1038/ncomms3575

“Addition of exogenous α-synuclein preformed fibrils to primary neuronal cultures to seed recruitment of endogenous a-synuclein to Lewy body and Lewy neurite–like aggregates”; Laura A. Volpicelli-Daley, Kelvin C. Luk and Virginia M.-Y. Lee; 2014; Nature Protocols;

http://www.nature.com/nprot/journal/v9/n9/full/nprot.2014.143.html

“Definition of a Molecular Pathway Mediating α-Synuclein Neurotoxicity”; Jacqueline Burré, Manu Sharma, and Thomas C. Südhof; 2015; The Journal of Neuroscience, 35(13):5221–5232