Principal Investigators

    Louise Berkhoudt Lassen


    Aarhus Universitet

    Contact information of lead PI



    Title of project or programme

    Investigating a-synuclein dependent neurodegeneration in two novel transgenic mouse lines modeling increased aggregation and lack of age-dependent trophic a-synuclein signalling

    Source of funding information


    Total sum awarded (Euro)

    € 282,509

    Start date of award


    Total duration of award in years



    Research Abstract

    Alpha-synuclein’s (a-syn) native state changes in the course of neurodegenerative synucleinopathies where it ultimately gets deposited in intracellular Lewy-like inclusions as filamentous aggregates. Soluble oligomeric aggregates are formed in the process of aggregation and are considered toxic species that cause a range of cell-autonomous effects and tissue responses thereby being responsible for the spreading degeneration of nerve cells characterizing the synucleinopathies. We have demonstrated that p25a stimulates aggregation of a-syn so we generated a mouse model of enhanced oligomer formation by expressing human p25a in forebrain neurons together with human a-syn from the Thy1 promoter (model I – Rosa26-p25a/Nex-Cre/Thy1-AS).

    Further information available at:

Types: Investments < €500k
Member States: Denmark
Diseases: N/A
Years: 2016
Database Categories: N/A
Database Tags: N/A

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