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Research & Development

Drosophila: Good model for drug discovery

--- by Dr. I.F. Peng, GM of Joekai

--- Jun 25, 2011

 

Flies look quite different from us, but they do display similar behavioral responses and share conserved biochemical mechanisms to human. Along the continuous fly studies for more than a century, scientists have been revealing that they can sleep in daily cycle, fight for space, food and/or mating, and learn/memorize favorites or dislikes. In certain conditions, flies also encounter similar social problems like us: drug addiction, alcoholism, and homosexual issue. These complicated phenotypic behaviors make flies a great tool in the drug discovery of neurodegenerative and neuropsychiatric disorders.   Both the effectiveness and cost are main factors in the industrial R&D. Fly operations are much cheaper than rodent and primate studies, and can be scaled up easily for high throughput screening in automated assay platforms. For instance, hundreds of compounds can be evaluated simultaneously for their effects on learning in the automated system developed by Joekai, in a very competitive price.


Drosophila models on Alzheimer's disease

--- by Mr. W.W. Ma, Deputy GM of Joekai

--- Oct 12, 2011  

Alzheimer’s disease (AD) afflicts approximately 15 million people worldwide, mainly at elder population. Due to the anticipated rapid growth of the elder populations, the AD patient population is expected to increase correspondingly. However, currently available AD treatments provide only symptomatic relief, temporarily improving brain function in patients. Agents/drugs with better improvements, especially on life expectation, are urgently needed from the enthusiastic market.  Dr. Yi Zhong, Professor of Tsinghua University, has been devoting to develop the platforms for AD drug discovery for more than a decade. His team choose an innovative animal model Drosophila (fruitfly), over-express human patients’ gene A-beta 42 in fruitflies, and carefully characterize patient-like syndromes in these transgenic animals (e.g., A-beta 42 accumulation in the brain, memory loss, pathological holes in brain, life span shortened, and etc…, refs #1 - #5). Joekai has acquired this carefully examined model for drug screening CRO services per clients’ needs.


Finding new cures for rare CNS disorders in Drosophila

--- by I.F. Peng, GM of Joekai

--- Dec 02, 2011  

There are diseases occurred only in a small portion of the population. Due to expected low financial returns, the development and commercialization of agents for these rare diseases have been strongly hurdled. Realistically, the cost of developing drugs for rare diseases sometimes can be higher than other diseases. There may be a way – by reducing the cost at early discovery phase -- to encourage developers initializing related programs and ultimately facilitate drug pipelines for patients.  The innovative way of using Drosophila models in CNS rare diseases can be quite cheaper than rodent and non-human primate systems. Joekai is also welcome co-developers to collaborate on other disease models.


References: 

(1) Iijima K, Liu HP, Chiang AS, Hearn SA, Konsolaki M, Zhong Y. (2004) Dissecting the pathological effects of human Abeta40 and Abeta42 in Drosophila: a potential model for Alzheimer's disease. Proc Natl Acad Sci U S A. 101(17):6623-8.

(2) Iijima-Ando K, Hearn SA, Granger L, Shenton C, Gatt A, Chiang HC, Hakker I, Zhong Y, Iijima K. (2008) Overexpression of neprilysin reduces alzheimer amyloid-beta42 (Abeta42)-induced neuron loss and intraneuronal Abeta42 deposits but causes a reduction in cAMP-responsive element-binding protein-mediated transcription, age-dependent axon pathology, and premature death in Drosophila. J Biol Chem. 283(27):19066-76.

(3) Iijima K, Chiang HC, Hearn SA, Hakker I, Gatt A, Shenton C, Granger L, Leung A, Iijima-Ando K, Zhong Y. (2008) Abeta42 mutants with different aggregation profiles induce distinct pathologies in Drosophila. PLoS One. 3(2):e1703. 

(4) Chiang HC, Iijima K, Hakker I, Zhong Y. (2009) Distinctive roles of different beta-amyloid 42 aggregates in modulation of synaptic functions. FASEB J. 23(6):1969-77.  

(5) Chiang HC, Wang L, Xie Z, Yau A, Zhong Y. (2010) PI3 kinase signaling is involved in Abeta-induced memory loss in Drosophila. Proc Natl Acad Sci U S A. 107(15):7060-5.