Blocking JNK Promising in SBMA

In a paper published in the July issue of Nature Neuroscience, Gerardo Morfini at the University of Illinois-Chicago and colleagues identified activation of a protein known as JNK as an important downstream effect of the underlying genetic mutation that leads to spinal-bulbar muscular atrophy (SBMA).

Activation of JNK, they say, may turn on a cell death program in the nervous system.

Although the underlying cause of SBMA is extra-long DNA on the X chromosome and subsequent production of an abnormal androgen receptor protein, the investigators say blocking JNK is a promising SBMA therapeutic target.