{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T01:27:00Z","timestamp":1789694820508,"version":"4.0.1"},"reference-count":46,"publisher":"Portland Press Ltd.","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,8,18]]},"abstract":"<jats:p>Saccharomyces cerevisiae (baker's yeast) is a well-established eukaryotic model organism, which has significantly contributed to our understanding of mechanisms that drive numerous core cellular processes in higher eukaryotes. Moreover, this has led to a greater understanding of the underlying pathobiology associated with disease in humans. This tractable model offers an abundance of analytical capabilities, including a vast array of global genetics and molecular resources that allow genome-wide screening to be carried out relatively simply and cheaply. A prime example of the versatility and potential for applying yeast technologies to explore a mammalian disease is in the development of yeast models for amyloid diseases such as Alzheimer's, Parkinson's and Huntington's. The present chapter provides a broad overview of high profile human neurodegenerative diseases that have been modelled in yeast. We focus on some of the most recent findings that have been developed through genetic and drug screening studies using yeast genomic resources. Although this relatively simple unicellular eukaryote seems far removed from relatively complex multicellular organisms such as mammals, the conserved mechanisms for how amyloid exhibits toxicity clearly underscore the value of carrying out such studies in yeast.<\/jats:p>","DOI":"10.1042\/bse0560085","type":"journal-article","created":{"date-parts":[[2014,8,18]],"date-time":"2014-08-18T11:18:39Z","timestamp":1408360719000},"page":"85-97","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Yeast models for amyloid disease"],"prefix":"10.1042","volume":"56","author":[{"given":"Barry","family":"Panaretou","sequence":"additional","affiliation":[{"name":"Institute of Pharmaceutical Science, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary W.","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Biology, National University of Ireland Maynooth, Maynooth, County Kildare, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2014,8,18]]},"reference":[{"key":"2021111610184230200_B1","doi-asserted-by":"crossref","first-page":"a008888","DOI":"10.1101\/cshperspect.a008888","article-title":"Genetics of Parkinson's disease","volume":"2","author":"Klein","year":"2012","journal-title":"Cold Spring Harb. 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