Name of Fellow


Institution


Funder


European Commission FP7-Seventh Framework Programme

Contact information of fellow


Country


EC

Title of project/programme


The role of neuronal intracellular traffic in Alzheimer´s disease

Source of funding information


European Commission FP7-Seventh Framework Programme

Total sum awarded (Euro)


€ 100,000

Start date of award


01/04/13

Total duration of award in years


4.0

The project/programme is most relevant to:


Alzheimer's disease & other dementias

Keywords


L302 Cell biology and molecular transport mechanisms |L502 Molecular and cellular neuroscience | | L404 Ageing |

Research Abstract


In neurons of Alzheimer’s disease (AD) there is an aberrant accumulation of beta-amyloid (A?) at synapses that renders difficult the formation of new memories for AD patients. Intracellular trafficking abnormalities have been implicated in A? accumulation. This research project aims to define how neuronal intracellular trafficking is mechanistically involved in A? accumulation that leads to AD. We will determine how the intracellular itinerary of the amyloid precursor protein in neurons influences the generation of A?. We will determine the intracellular trafficking of lysosomal hydrolases in neurons and their contribution to the lysosomal clearance of A?. Furthermore, we will investigate the mechanism whereby regulators of intracellular trafficking identified as risk-factors for AD contribute to A? accumulation. Finally, because aging is the most important risk factor for AD, we will determine if alterations in intracellular trafficking occur in aging, identifying a new mechanism of vulnerability to neurodegeneration in AD. Thus, we will demonstrate how intracellular trafficking is implicated in AD and unravel an important disease mechanism.

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