Principal Investigators

    BERGER, CHRISTOPHER L.

    Institution

    UNIVERSITY OF VERMONT & ST AGRIC COLLEGE

    Contact information of lead PI

    Country

    USA

    Title of project or programme

    Tau-mediated regulation of axonal transport

    Source of funding information

    NIH (NIA)

    Total sum awarded (Euro)

    € 1,430,245.87

    Start date of award

    01/07/2013

    Total duration of award in years

    4

    The project/programme is most relevant to:

    Alzheimer's disease & other dementias

    Keywords

    Axonal Transport, tau Proteins, Kinesin, Microtubules, FTD with parkinsonism

    Research Abstract

    Tau is a microtubule associated protein (MAP) primarily expressed in neurons that has traditionally been thought to promote microtubule assembly and stability in the axon. However, recent in vitro motility experiments have also demonstrated that tau is a potent inhibitor of processive kinesin movement along microtubules. These results present an interesting paradox, namely – how can kinesin processively transport its cargo along microtubules in the presence of tau, which is highly expressed in neurons and localized to the axon? The answer to this question has important implications for axonal transport, a critical process in neurons required for the efficient delivery of organelles, proteins, nucleic acids, and small molecules synthesized in the cell body to their site of function in distal regions of the axon. Defects in any one of the protein components in the axonal transport machinery, which includes microtubules, members of the kinesin superfamily of motor proteins, a variety of adapter molecules that link kinesin to its intracellular cargo, and MAPs such as tau, result in serious and often lethal neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s, and ALS. This proposal will test the hypothesis that tau is a conformationally dynamic protein that can adopt multiple modes of interaction with different nucleotide states of the microtubule lattice. Furthermore, the mechanistic basis for isoform specific differences in tau’s function will also be examined, with an emphasis its ability to modulate the processive motility of kinesin-1, the major molecular motor involved in axonal transport.

    Lay Summary

    Defects in any one of the protein components in the axonal transport machinery, such as the microtubule associated proteins tau, result in serious and often lethal neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s, and ALS. Thus understanding tau’s role in modulating kinesin-1 (a major molecular motor protein in the axon) function in the neuron is imperative to elucidating the molecular mechanisms of axonal transport in both normal and pathological states.

    Further information available at:

Types: Investments > €500k
Member States: United States of America
Diseases: Alzheimer's disease & other dementias
Years: 2016
Database Categories: N/A
Database Tags: N/A

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