Functional analysis of axonal transport vesicles containing APP, APLP1 or APLP2

• Antragsteller: Professor Dr. Stefan Kins
• Fachliche Zuordnung: Molekulare Biologie und Physiologie von Nerven- und Gliazellen
• Förderung: Förderung von 2002 bis 2008
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 5385113

Axonal transport emerge to represent a common feature in the etiology of several neurodegenerative diseases, such as Huntington's disease, Parkinson's disease, frontotemporal dementia, Creutzfeldt-Jacob disease and Alzheimer's disease (AD). Pathologically, AD is characterized by neurodegeneration, intracellular neurofibrillary tangles and extracellular plaques composed mainly of the beta Amyloid peptide, derived from the amyloid precurser protein (APP). Recent evidence suggests that APP mediates axonal transport, since a function for APP as membrane receptors of the motor protein kinesin-I was postulated. We want to determine if the APP-like proteins APLP1 and APLP2, which are expected to have a similar function, also mediate transport and interact with components of the kinesin motor protein complex. Certain proteins seem to be transported along the axon specifically in those vesicles designated by APP, suggesting in regard to the postulated ovelapping functions of the APP-family members, that APLP1 and APLP2 mediate the transport of another class of vesicles containing identical but also unique cargo proteins. The identification of these cargo proteins is our major goal. These analyses will help to clarify the function of APP-family members under physiological conditions and in the pathology of AD.

• DFG-Verfahren: Schwerpunktprogramme
• Teilprojekt zu: SPP 1085: Zelluläre Mechanismen der Alzheimer Erkrankung
• Beteiligte Person: Professor Dr. Konrad Beyreuther