ERA-NET Neuron Abeta ID
ERA-NET – Network of European Funding for Neuroscience Research
The objective of ERA-NET is to reduce fragmentation across the European Research Area (ERA) by initiatives to develop and strengthen the coordination of national and regional research programmes.
This initiative of ERA-NET supports basic, clinical and translational research in disease-related neuroscience. Neurological diseases are highly prevalent and our understanding of their pathogenesis is still limited. Effective therapeutics and also diagnostics, particularly early or even predictive ones, are largely lacking. They are sorely needed to relieve the burden of those suffering from mental disorders like depression or schizophrenia as well as the growing numbers of patients of neurodegenerative diseases, like Alzheimer or Parkinson.
ERA-NET Neuron ABETA ID
ABETA ID is a project in the Joint Transnational Call 2012 “Novel Methods and Approaches towards the Understanding of Brain Diseases” funded from 2013 to 2016.
The hypothesis underlying our research activities in ABETA ID is that small, seeding-competent amyloid-beta species are crucial to pathogenesis in Alzheimer’s disease. With an integrated array of methods we want to make these species available for experimental studies in model systems towards an improved understanding of the role of amyloid-beta aggregation in Alzheimer’s disease and to facilitate the discovery of novel therapeutic leads.
The project partners are:
Erich Wanker (Coordinator)
Max-Delbrück-Centrum für Molekulare Medizin (MDC) Berlin-Buch, Germany
Bieschke et al. (2012) Small-molecule conversion of toxic oligomers to nontoxic beta-sheet-rich amyloid fibrils. Nat. Chem. Biol. 8(1):93-101.
Bart De Strooper
VIB Center for the Biology of Disease, Center for Human Genetics, KU Leuven, Belgium
Benilova et al. (2012) The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes. Nat. Neurosci. 15(3):349-57.
Inserm U837 – JPArc,
University of Lille, France
Brouillette et al. (2012) Neurotoxicity and memory deficits induced by soluble low-molecular-weight amyloid-ß1-42 oligomers are revealed in vivo by using a novel animal model. J. Neurosci. 32(23): 7852–7861.
Department of Angiocardioneurology, IRCCS Neuromed
Carnevale et al. (2012) Hypertension induces brain β-amyloid accumulation,cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature. Hypertension 60(1):188-97.
CERM University of Florence, Sesto Fiorentino, Italy
Bertini et al. (2013) Formation kinetics and structural features of Beta-amyloid aggregates by sedimented solute NMR. Chembiochem. 14(14):1891-7.
The papers cited are exemplary studies of the partner labs regarding their research in ERA-NET Neuron ABETA ID.