Making mouse diseases more like human diseases

mouseIt is almost impossible to study basic cellular mechanisms in humans. This is why scientists spend so much time trying to find animal models for human diseases. Sometimes, there is a naturally occurring disease in animals that is analogous to  a human condition. Other times, the animal’s genome can be modified to replicate mutations that are found in human diseases. However, despite the best efforts of many scientists, models often fail to faithfully replicate all aspects of human disease.

This led to the creation of a new mouse model of spontaneously developing Creutzfeldt-Jakob disease (CJD) by the Lindquist lab at MIT. Continue reading “Making mouse diseases more like human diseases”

Breaking in Order to Build

Image courtesy of the Journal of Cell Biology
Image of labeled (red) DNA breaks in a single cell courtesy of the Journal of Cell Biology

Do you ever think about how every time you encounter something new your brain adjusts and rewires and makes molecular changes so you can remember this new object in the context of what you already know? I know I do, though that may be a by-product of my neuroscience upbringing. Even if you don’t think about it, it’s happening. Complex changes in the numbers and amounts of gene expression are critical to developing and maintaining memories. And as it turns out, breaking the DNA in your brain cells into pieces is also part of the process.

Continue reading “Breaking in Order to Build”

Coming to news stands. . .

Needless to say (but I’m going to anyway), I am pleased as punch that my lab’s most recent offering unto the body of scientific literature (“Analysis of alternative splicing associated with aging and neurodegeneration in the human brain”) was put on the cover of the current issue of Genome Research. In this paper, we investigated the connections between alternative splicing profiles in the aging brain and in brains suffering from neurodegenerative disorders, like Alzheimer’s disease. It is important to note that we were characterizing the alternative splicing differences associated with aging and disease, not identifying splicing changes that cause the diseases or the symptoms. Such questions will require ongoing work, which this study will, hopefully, help guide. Continue reading “Coming to news stands. . .”

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