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 on Computational Neuroscience (#1055858) at the
Department of Neurobiology of the University of Rome
"La Sapienza" will begin Wednesday Oct.7th 2020.
Class schedule: 09:00-13:00, every Wed,
and Thurs. until Nov.26th.
Students interested in taking the course are kindly invited
to contact Michele Migliore.
More info on the course can be found
here
.
International Collaborations
Yale University School of Medicine Department of Neuroscience
P.O. Box 208001, New Haven, CT 06520-8001, USA
University of Naples Federico II Department of Mathematics
via Cintia, Naples, Italy
University of Naples Federico II Department of Neuroscience
via Pansini 5, 80131 Naples, Italy
Heinrich Heine University Department of Neuro- and Sensory Physiology
Universitätsstraße 1, 40225 Düsseldorf, Germany
European Brain Research Institute
via del Fosso di Fiorano 64, 00143 Rome, Italy
University of Palermo Department of Mathematics and Computer Science
via Archirafi, Palermo, Italy
IPMC - CNRS
UMR7275, Valbonne, France
Otto-von-Guericke-University Magdeburg Institute of Physiology
Leipziger Str. 44, Haus 28 39120 Magdeburg, Germany
External Funding
The
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.
The CircProt project
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.
