SRI 7th International Conference
Neurodegeneration in Alzheimer’s Disease; Parkinson’s Disease & Related Disorders
April 18-19, 2005

Hereditary Disease Foundation 2004 Conference
August 12-15, 2004

34th Annual Society for Neuroscience Conference
October 23-27, 2004

Cold Spring Harbor Laboratory Meeting
Drug Discovery in Neurodegenerative Diseases
December 2-5, 2004


1. Drosophila is a validated model system for neurodegenerative diseases


Whitworth AJ, Wes PD, Pallanck LJ
Drosophila models pioneer a new approach to drug discovery for Parkinson’s disease.
Drug Discov Today. 2006 Feb;11(3-4):119-26
Zoghbi, HY and Botas, J
Mouse and fly models of neurodegeneration.
Trends Genet. (2002) 18:463-71

Lansbury, PT Jr.
Back to the future: the ’old-fashioned’ way to new medications for neurodegeneration.
Nat Med. (2004) 10 Suppl:S51-7

Primary publications:

Greeve I, Kretzschmar D, Tscha¨pe J-A, Beyn A, Brellinger C, Schweizer M, Nitsch RM, Reifegerste R
Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila. J. Neurosci. (2004) 24:3899-3906

Expression of human APP and human b-secretase in Drosophila results in Ab42 amyloidogenic processing of APP, amyloid plaque formation, and age-dependent neurodegeneration.

Ravikumar B, Vacher C, Berger Z, Davies JE, Luo S, Oroz LG, Scaravilli F, Easton DF, Duden R, O’Kane CJ, Rubinsztein DC.

Inhibition of mTOR induces autophagy and reduces toxicity of polyglutamine expansions in fly and mouse models of Huntington disease.

Nat Genet. (2004) 36(6):585-95. Epub 2004 May 16
Sequestration of mTOR protects against polyglutamine toxicity. The specific mTOR inhibitor rapamycin protects against neurodegeneration in a fly model of Huntington disease, and the rapamycin analog CCI-779 improved performance on four different behavioral tasks and decreased aggregate formation in a mouse model of Huntington disease.

Jackson GR, Wiedau-Pazos M, Sang TK, Wagle N, Brown CA, Massachi S, Geschwind DH.
Human wild-type tau interacts with wingless pathway components and produces neurofibrillary pathology in Drosophila.
Neuron. 2002 May 16;34(4):509-19.

2. Drosophila genome sequenced and annotated

Hild M, Beckmann B, Haas SA, Koch B, Solovyev V, Busold C, Fellenberg K, Boutros M, Vingron M, Sauer F, Hoheisel JD, Paro R.

An integrated gene annotation and transcriptional profiling approach towards the full gene content of the Drosophilagenome.
Genome Biol. (2003) 5(1):R3. Epub 2003 Dec 22

Reiter LT, Potocki L, Chien S, Gribskov M, Bier E
A systematic analysis of human disease-associated gene sequences in Drosophila melanogaster.
Genome Res. (2001) 11:1114-25

3. Compounds improve disease phenotypes in Drosophila and mice

Micchelli CA, Esler WP, Kimberly WT, Jack C, Berezovska O, Kornilova A, Hyman BT, Perrimon N, Wolfe MS.
Gamma-secretase/presenilin inhibitors for Alzheimer’s disease phenocopy Notch mutations in Drosophila.
FASEB J. (2003) 17:79-81. Epub 2002 Nov 01

Hendricks JC, Kirk D, Panckeri K, Miller MS, Pack AI.
Modafinil maintains waking in the fruit fly Drosophila melanogaster.
Sleep. 2003 Mar 15;26(2):139-46

Fruit flies exhibit a sleep-like rest state that shares behavioral characteristics with mammalian sleep, including a homeostatic increase in rest after deprivation by mechanical methods. Modafinil, a novel wake-promoting agent, affects states of arousal in Drosophila in the same direction as it does in mammals.

Pendleton, RG, Parvez, F, Sayed, M, and Hillman, R
Effects of pharmacological agents upon a transgenic model of Parkinson’s disease in Drosophila melanogaster.
J. Pharmacol. Exp. Ther. (2002) 300:91-96. (Erratum: J. Pharmacol. Exp. Ther. (2002) 300:1131)
Drugs with different mechanisms of action improve motor function in aDrosophila model of Parkinson’s Disease.

Steffan, JS, Bodai, L, Pallos, J, Poelman, M, McCampbell, A, Apostol, BL, Kazantsev, A, Schmidt, E, Zhu, YZ, Greenwald, M, Kurokawa, R, Housman, DE, Jackson, GR, Marsh, JL & Thompson, LM

Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila.
Nature (2001) 413: 739-43

4. Use of Drosophila disease models beyond neurodegeneration

Hendricks JC, Sehgal A.
Why a fly? Using Drosophila to understand the genetics of circadian rhythms and sleep.
Sleep (2004) 27(2):334-42

Potter CJ, Turenchalk GS, Xu T
Drosophila in cancer research. An expanding role.
Trends Genet. (2000) 16(1):33-9. Review
A general review on Drosophila as a model to study cancer

Bellen, H
The Fruit Fly: A model organism to study the genetics of alcohol abuse and addiction?
Cell (1998) 93:909-912