Dying for a cause: invertebrate genetics takes on human neurodegeneration.
If invertebrate neurons are injured by hostile environments or aberrant proteins they die much like human neurons, indicating that the powerful advantages of invertebrate molecular genetics might be successfully used for testing specific hypotheses about human neurological diseases, for drug discovery and for non-biased screens for suppressors and enhancers of neurodegeneration. Recent molecular dissection of the genetic requirements for hypoxia, excitotoxicity and death in models of Alzheimer disease, polyglutamine-expansion disorders, Parkinson disease and more, is providing mechanistic insights into neurotoxicity and suggesting new therapeutic interventions. An emerging theme is that neuronal crises of distinct origins might converge to disrupt common cellular functions, such as protein folding and turnover.
Driscoll
Monica
M
Department of Molecular Biology and Biochemistry, Rutgers, The State University of New Jersey, A232 Nelson Biological Laboratories, 604 Allison Road, Piscataway, New Jersey 08855, USA. driscoll@mbcl.rutgers.edu
Gerstbrein
Beate
B
D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology; D000818:Animals; D030801:Animals, Genetically Modified; D017173:Caenorhabditis elegans / Q000166:cytology / Q000235:genetics; D016923:Cell Death; D004331:Drosophila melanogaster / Q000166:cytology / Q000235:genetics; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000473:pathology; D007448:Invertebrates / Q000166:cytology / Q000235:genetics*; D007473:Ion Channels / Q000378:metabolism; D008959:Models, Neurological; D009154:Mutation; D009410:Nerve Degeneration / Q000235:genetics* / Q000473:pathology*; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D010300:Parkinson Disease / Q000235:genetics / Q000473:pathology; D010455:Peptides / Q000235:genetics
D007473:Ion Channels; D010455:Peptides; C097188:polyglutamine