In a recent study encompassing the use of fruit flies, scientists at VIB, headquartered in Flanders, Belgium, and KU Leuven, Belgium, say they have demonstrated that over-activity of the enzyme HDAC6 in the nerve ends aggravates symptoms of amyotrophic lateral sclerosis (ALS).

Patrik Verstreken, PhD, VIB/KU Leuven, emphasizes the study’s importance, “…Any additional insight into the dysfunction of nerve cells and the defective transmission of signals to the muscles paves the way to further targeted ALS research.”

According to a recent news release, Verstreken and colleagues have investigated how this type of nerve cell becomes defective in fruit flies that express a form of ALS. The specific defect in ALS is found at the nerve endings, and this is reportedly where the team pinpointed an over-activity of HDAC6. The release notes that the disrupted synaptic transmission is attributed to the over-activity of HDAC6, resulting in a symptomatic aggravation of the disease.

The results suggest, in theory, that to stop the process it may be key to combat the over-activation of HDAC6 in order to return to the “normal” activity of the HDAC6 enzyme. As stated in the release, while the study’s findings may pave the way for symptomatic ALS treatment in the future, the HDAC6 defect is likely one of many enzyme defects that play a role in ALS. Verstreken and Wim Robberecht, VIB/KU Leuven, also demonstrated the enzyme Elp3 behaves in the same process at the nerve endings as HDAC6. The researchers ultimately call for a variety of avenues to be explored in order to find a treatment for ALS.

Source: Medical News Today, VIB, KU Leuven