Sandal Strap KRISTIN Platform Ankle White Block Heel We are interested in understanding how the brain works. For this purpose, we use the available experimental data to design, implement and analyze realistic models of neurons, synapses, and networks. The goal is to uncover the mechanisms underlying higher brain functions, to help the development of innovative therapies to treat brain diseases and dysfunctions. The list of scientific publications will give you an idea of how we do that.
The course Cybernetics (#02006) is active at the
Department of Mathematics and Informatics of the University of Palermo for the second semester (05 Mar - 07 June 2018). Class schedule: 14:30-17:00, monday and thursday. Students interested in taking the course are kindly invited to contact Michele Migliore. More info can be found
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The course on Computational Neuroscience (#1055858) at the
Department of Neurobiology of the University of Rome "La Sapienza" will begin Wednesday Oct.3rd 2018. Class schedule: 09:00-13:00, on Oct.3, 4, 10, 11, 24, and 25. Students interested in taking the course are kindly invited to contact Michele Migliore. More info on the course can be found
Otto-von-Guericke-University Magdeburg Institute of Physiology Heel KRISTIN Sandal Ankle Block Strap Platform White Leipziger Str. 44, Haus 28 39120 Magdeburg, Germany
Human Brain Project (HBP) is a European Commission Future and Emerging Technologies Flagship. The HBP aims to put in place a cutting-edge, ICT-based scientific Research Infrastructure for brain research, cognitive neuroscience and brain-inspired computing. The Project promotes collaboration across the globe, and is committed to driving forward European industry.
Short Wedges Shoes Boots Platform Women's Concise Wine Bandage Carol Single Color Red q618c8Fw focuses on synaptic circuit protection in Alzheimers’s disease (AD) and Hunting-tion’s disease (HD). Alzheimer’s and Huntington’s disease result from the erroneous communication of neurons at synapses in different brain areas (neocortex, hippocampus, striatum). The protein BDNF regulates synaptic communication under healthy conditions. However, insufficient release of BDNF from neurons and defective BDNF signaling in target neurons contribute to cellular malfunctions in AD and HD. Although they are essential to the development of effective therapies, the underlying molecular mechanisms for deficits in synaptic communication in these diseases are not understood.