RE: Removing lysosomal aggregates; obviating mitochondrial mutations (was: specific amino acid...)

From: Adrian Tymes (wingcat@pacbell.net)
Date: Sat Apr 26 2003 - 10:28:17 MDT

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    --- "Robert J. Bradbury" <bradbury@aeiveos.com> wrote:
    >
    http://www.sciencemag.org/cgi/content/abstract/300/5619/636
    >
    > I don't have access to Science otherwise I'd post
    > the abstract.
    > It also doesn't appear to have made it into PubMed
    > yet...

    Happy to oblige.

    Alpha-synuclein ({alpha}-syn) and tau polymerize into
    amyloid fibrils and form intraneuronal filamentous
    inclusions characteristic of neurodegenerative
    diseases. We demonstrate that {alpha}-syn induces
    fibrillization of tau and that coincubation of tau and
    {alpha}-syn synergistically promotes fibrillization of
    both proteins. The in vivo relevance of these findings
    is grounded in the co-occurrence of {alpha}-syn and
    tau filamentous amyloid inclusions in humans, in
    single transgenic mice that express A53T human
    {alpha}-syn in neurons, and in oligodendrocytes of
    bigenic mice that express wild-type human {alpha}-syn
    plus P301L mutant tau. This suggests that interactions
    between {alpha}-syn and tau can promote their
    fibrillization and drive the formation of pathological
    inclusions in human neurodegenerative diseases.



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