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ABINEP M2-project 3: Modellierung Dopamin-induzierter neuronaler Netzwerk-Aktivität / "Learning conditional associations: rich temporal context and involvement of hippocampus / medial temporal lobe"
M.Sc. Ehsan Kakaei
EU - ESF Sachsen-Anhalt ;
EUROPÄISCHE UNION - ESF -  Europäischer Sozialfonds
The international Graduate school (GS) on Analysis, Imaging, and Modelling of Neuronal and Inflammatory Processes (ABINEP) is based on the two internationally recognized biomedical research foci of the Otto-von-Guericke-University Magdeburg (OVGU), Neurosciences and Immunology. ABINEP aims at fostering cutting edge research projects in rising sub-disciplines of these research areas, which are currently supported by several German Research foundation (DFG)- and European Community (EU)-funded collaborative projects in Magdeburg (including the DFG-funded Collaborative Research Centers SFBs 779 and 854 and associated graduate schools, as well as DFG TRRs 31 and 62). The program includes scientists from the Medical Faculty/ University Hospital Magdeburg (MED) and the Faculty of Natural Sciences (FNW) of the OVGU, the Institute for Neurobiology (LIN) and German Center for Neurodegenerative Diseases (DZNE), both located in Magdeburg, the Helmholtz Centre of Infection Research in Braunschweig as well as international collaborators.

To further strengthen the international interconnection of these research foci, 21 projects were defined to educate excellent international PhD student candidates in any of the 4 ABINEP topical modules:
1) Neuroinflammation: Inflammatory processes in neurodegeneration
2) Neurophysiology and Computational Modelling of Neuronal Networks
3) Immunosenescence: Infection and immunity in the context of aging
4) Human Brain Imaging for diagnosing neurocognitive disorders

2) Neurophysiology and Computational Modelling of Neuronal Networks
Sport can activate protective mechanism which suppresses Dementia outbreaks. The detailed principles and possibilities to optimize therapies are not yet known. It is assumed that substances such as brain-derived neurotrophic factor (BDNF) and dopamine are mobilized in brains and increase synaptic plasticity processes and therefore to a delay in Dementia outbreaks. A systematical evaluation of the altered synaptic plasticity and the communication between different brain regions by BDNF and dopamine is currently missing and requires now scientific approaches. Computational modelling of neuronal networks should be used to predict the influence of pharmacological substances on the brain network activity and thereby the suppression of dementia outbreaks within animal models.

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