New Drug Targets Lou Gehrig’s Disease
By Ivanhoe Health Correspondent Melissa Colón
(Ivanhoe Newswire) – More than 90 percent of Lou Gehrig’s disease cases have no genetic cause or family history. According to a recent study, two proteins conspire to promote a lethal neurological disease.
Since 2006, researchers have known that the protein TDP-43 is in involved in amyotrophic later sclerosis, ALS, also known as Lou Gehrig’s disease, a neurodegenerative disorder that results in progressing loss of motor function and ultimately death.
“In this article, we report for the first time that TDP-43 interacts with and activates a protein called NF-kB p65 which is a key regulator for the synthesis of a number of factors associated with innate immunity and inflammation,” said Jean-Pierre Julien, PhD, Biochemistry, Senior Canada Research Chair in Neurodegeneration, Laval University, Quebec.
Furthermore, Jean-Pierre Julien and his colleagues at Laval University in Quebec found through examination of post-mortem spinal cord samples that the activation of the inflammatory protein NF-kB pathway was detected in ALS motor neurons and not only in immune cells. Through the use of a mouse model of ALS, this discovery showed that an inhibitor of NF-kB pathway could weaken disease symptoms.
“The good news for ALS patients is that therapeutic interventions to target this pathway are conceivable. However, we must keep in mind that NF-kB inhibitors will have to be tested cautiously so as not to compromise our healthy—and necessary-- immune responses,” said Julien.
One of the goals of Julien and his colleagues will be to develop a drug treatment that can specifically target the interaction between TDP-43 andNF-kB p65.
SOURCE: Jean-Pierre Julien, Interviewed November 16, 2011