TY - JOUR
T1 - Neurodegenerative mutants in Drosophila
T2 - A means to identify genes and mechanisms involved in human diseases?
AU - Kretzschmar, Doris
N1 - Funding Information:
Acknowledgements I would like to thank B. Poeck for the critical reading of the manuscript. Special thanks are due to M. Palladino, K. Finley, as well as M. Chao and J. Rosenbluth for providing the figure material. Funding for the work in the author’s laboratory is provided by the National Institute of Health, the Medical Research Foundation of Oregon, and the Alzheimer Foundation Initiative, Germany.
PY - 2005/11
Y1 - 2005/11
N2 - There are 50 ways to leave your lover (Simon 1987) but many more to kill your brain cells. Several neurodegenerative diseases in humans, like Alzheimer's disease, have been intensely studied but the underlying cellular and molecular mechanisms are still unknown for most of them. For those syndromes where associated gene products have been identified their biochemistry and physiological as well as pathogenic function is often still under debate. This is in part due to the inherent limitations of genetic analyses in humans and other mammals and therefore experimentally accessible invertebrate in vivo models, such as Caenorhabditis elegans and Drosophila melanogaster, have recently been introduced to investigate neurodegenerative syndromes. Several laboratories have used transgenic approaches in Drosophila to study the human genes associated with neurodegenerative diseases. This has added substantially to our understanding of the mechanisms leading to neurodegenerative diseases in humans. The isolation and characterization of Drosophila mutants, which display a variety of neurodegenerative phenotypes, also provide valuable insights into genes, pathways, and mechanisms causing neurodegeneration. So far only about two dozen such mutants have been described but already their characterization reveals an involvement of various cellular functions in neurodegeneration, ranging from preventing oxidative stress to RNA editing. Some of the isolated genes can already be associated with human neurodegenerative diseases and hopefully the isolation and characterization of more of these mutants, together with an analysis of homologous genes in vertebrate models, will provide insights into the genetic and molecular basis of human neurodegenerative diseases.
AB - There are 50 ways to leave your lover (Simon 1987) but many more to kill your brain cells. Several neurodegenerative diseases in humans, like Alzheimer's disease, have been intensely studied but the underlying cellular and molecular mechanisms are still unknown for most of them. For those syndromes where associated gene products have been identified their biochemistry and physiological as well as pathogenic function is often still under debate. This is in part due to the inherent limitations of genetic analyses in humans and other mammals and therefore experimentally accessible invertebrate in vivo models, such as Caenorhabditis elegans and Drosophila melanogaster, have recently been introduced to investigate neurodegenerative syndromes. Several laboratories have used transgenic approaches in Drosophila to study the human genes associated with neurodegenerative diseases. This has added substantially to our understanding of the mechanisms leading to neurodegenerative diseases in humans. The isolation and characterization of Drosophila mutants, which display a variety of neurodegenerative phenotypes, also provide valuable insights into genes, pathways, and mechanisms causing neurodegeneration. So far only about two dozen such mutants have been described but already their characterization reveals an involvement of various cellular functions in neurodegeneration, ranging from preventing oxidative stress to RNA editing. Some of the isolated genes can already be associated with human neurodegenerative diseases and hopefully the isolation and characterization of more of these mutants, together with an analysis of homologous genes in vertebrate models, will provide insights into the genetic and molecular basis of human neurodegenerative diseases.
UR - http://www.scopus.com/inward/record.url?scp=27144488101&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=27144488101&partnerID=8YFLogxK
U2 - 10.1007/s10158-005-0005-8
DO - 10.1007/s10158-005-0005-8
M3 - Review article
C2 - 16187075
AN - SCOPUS:27144488101
SN - 1354-2516
VL - 5
SP - 97
EP - 109
JO - Invertebrate Neuroscience
JF - Invertebrate Neuroscience
IS - 3-4
ER -