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Learning from mistakes: Cholinergic modulation of interactions between performance monitoring and long-term memory
Finanzierung:
Deutsche Forschungsgemeinschaft (DFG) ;
This project is part of the Research Training Group (RTG) 2413 "The aging synapse (SynAGE)"
Cf. http://gp.cbbs.eu/synage-tp13/
RTG 2413: The Aging Synapse - Molecular, Cellular and Behavioral Underpinnings of Cognitive Decline
Our aging society has benefitted in large from advances in modern medicine in the last century. By 2050 the global number of elderly dependent people will supposedly have reached 277 million (Prince et al., 2013) with approximately every fourth Western citizen being over the age of 65 (Cracknell, 2010). This demographic change poses an increasing burden with incurred economic, infrastructural, and last but not least large social expenses - especially if it comes down to decline of cognitive function in the elderly. Thus, there is an urgent need for a better understanding of such cognitive decline in order to develop strategies for maintaining and improving mental health and quality of life in the elderly population. Current research in this field focuses mainly on dementia and associated neurodegenerative diseases. Much less investigated and in many aspects neglected, however, are the consequences of normal aging as such for synaptic, cellular and neuronal network properties. Normal aging is associated with a decline in sensory, motor, and cognitive function, in particular working memory, cognitive flexibility and multi-tasking capacity, and although relatively mild as compared to dementia, this negatively impacts on health and life quality. In fact, there is cumulating evidence that not only genetic factors contribute to the course of aging but also individual lifestyle habits such as rich diet, little to no exercise, stress, provoked development of the metabolic syndrome, vascular alterations, all of which negatively impact on cognitive function in the elderly as well.
The innovative research program of RTG2413 SynAGE deals with the idea that cognitive decline in normal aging results from subtle synaptic alterations that impart an imbalance between stability and plastic properties of spine synapses and that is qualitatively different from neurodegeneration. This will further involve changes in the properties and functionality of the extracellular matrix, communication and interaction with glia cells and cells of the immune system, neuromodulation, and ultimately otherwise compensatory mechanisms. We aim to understand these processes of synaptic aging from a molecular, cellular as well as behavioral angle by jointly addressing transversal, intimately linked themes forming a comprehensive framework for inspiring thesis projects with high societal relevance.
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