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Researcher Marc Vermulst and his team have discovered how years of prion-like proteins cause neurodegenerative disorders.

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He explains

  • That while the copying of 3 billion base pairs inevitably lead to mistakes, certain mistakes are more significant;
  • Why those mistakes are not evident for years; and
  • Why a particular copying mistake leads to a misfolded protein that can take on a life of its own, causing diseases connected with the human aging process.

Marc Vermulst is an assistant professor of gerontology at the University of Southern California. He has had a lifelong interest in the human aging process and signs of aging and studies how our genome changes. He measures that change and works to understand how this impacts our health.

Early in his career while studying premature aging syndromes, he noted that most were characterized by an instable genome—in other words, these early signs of aging were accompanied by a genome that faced changes at a faster pace than most normal genomes. This pushed him to his current interest in genome change and aging.

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He’s been trying to link the natural aging process in a mechanistic way to age-related diseases. He comments that while we see those disease occur as a result of the aging process, what exactly is happening to cause those diseases has not been clear; however, his work has identified what they think may be a key cause, namely misfolded proteins that lead to prion-like proteins, which result from transcription errors.

These proteins take on a life of their own and force other proteins to conform to their shape, a shape that seems to be toxic to cells. He explains this process in more detail and suggest long term goals these findings may address such as medically relevant therapies.

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For more, see his website:

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