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Over-activity of enzyme HDAC6 exacerbates symptoms of Amyotrophic Lateral Sclerosis
Date:6/26/2014

ting in a symptomatic exacerbation of the disease. In order to stop this process, it would in theory be helpful to combat the over-activation of the enzyme HDAC6 in order to return to "normal" activity of the HDAC6 enzyme.

Not only HDAC6 defect

Although this discovery may provide a possible avenue for symptomatic ALS treatment, it should be noted that the HDAC6 defect is probably one of the many enzyme defects that play a role in ALS. Previously, Patrik Verstreken and Wim Robberecht (VIB/KU Leuven) demonstrated that another enzyme that is involved in ALS Elp3 acts on the same process at the nerve endings as HDAC6. Ideally, the various avenues should all be studied in the hope of finding a treatment for ALS in the future.


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Contact: Sooike Stoops
sooike.stoops@vib.be
32-924-46611
VIB (the Flanders Institute for Biotechnology)
Source:Eurekalert

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