A new mouse model developed by Harvard Medical School researchers and reported in the October 30 Neuron may allow scientists for the first time to spotlight two key proteins in a living animal and see how they contribute to the neuronal death and atrophy found in neurodegenerative diseases. The two proteins are dubbed p25 and cyclin-dependent kinase 5 (Cdk5).
"This is an excellent animal model for any therapeutic approach toward p25 and its link to Alzheimers and similar neurodegenerative diseases," says Li-Huei Tsai, HMS professor of pathology and Howard Hughes Medical Institute associate investigator, the studys lead author. "We know that p25 causes neurodegeneration, and we want to figure out how that mechanism works."
The new model is the latest in Cdk5 research from the lab of Li-Huei Tsai. Over the past nine years, Tsai and her colleagues have defined many of Cdk5s functions and noted the role its usual regulator p35 plays in orienting neuronal migration and growth. Their latest challenge is deciphering how Cdk5 and the pernicious regulator p25 lead to neurodegenerative diseases.
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