Project C04

Apraxia in Alzheimer’s disease: Plastic reorganization of praxis networks in response to chronically progressive dysfunction

Project C04 studies the molecular and functional mechanisms underlying neurodegeneration-induced apraxia and its counteracting reserve mechanisms based on the hypothesis that apraxic deficits in Alzheimer’s disease (AD) are associated with the location and extent of tau-pathology in praxis-related cortical networks. Characterizing apraxia in AD at the behavioural (neuropsychological profiling, including the Cologne apraxia screening, KAS), molecular (Tau-PET imaging), and functional (resting-state fMRI) levels will provide fundamental insights into higher motor functions and may identify specific factors contributing to resilience against apraxia.

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Alexander Dzrezga

Principal Investigator

 

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Gerard N. Bischof

Postdoc

 

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Peter Weiss-Blankenhorn

Principal Investigator

 

 

 

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Arman Smakic

Clinician Scientist

 

 

 

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