Functional genomics approaches to neurodegenerative diseases.
Many of the neurodegenerative diseases that afflict humans are characterised by the protein aggregation in neurons. These include complex diseases like Alzheimer's disease and Parkinson's disease, and Mendelian diseases caused by polyglutamine expansion mutations [like Huntington's disease (HD) and various spinocerebellar ataxias (SCAs), like SCA3]. A range of functional genomic strategies have been used to try to elucidate pathways involved in these diseases. In this minireview, I focus on how modifier screens in organisms from yeast to mice may be of value in helping to elucidate pathogenic pathways.
Rubinsztein
David C
DC
Department of Medical Genetics, Addenbrooke's Hospital, Cambridge Institute for Medical Research, Wellcome/MRC Building, Hills Road, Cambridge, CB2 2XY, UK. dcr1000@hermes.cam.ac.uk
D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics; D004195:Disease Models, Animal; D004330:Drosophila / Q000235:genetics; D023281:Genomics; D020271:Heredodegenerative Disorders, Nervous System / Q000209:etiology / Q000235:genetics*; D006801:Humans; D008322:Mammals / Q000235:genetics; D008957:Models, Genetic; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000235:genetics; D012441:Saccharomyces cerevisiae / Q000235:genetics
D009419:Nerve Tissue Proteins