Huntington’s disease research news. In plain language. Written by scientists. For the global HD community.

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Articles with the topic: gene-silencing

Lost in translation? New insights into the making of the Huntington's disease protein

Lost in translation? New insights into the making of the Huntington's disease protein

Melissa Christianson on April 01, 2013

Everyone has two copies of the huntingtin gene but Huntington's disease is caused by a copy that's extra-long. New research shows that cells have different controls for how the normal and extra-long instructions are used to make protein. These controls on the protein-making process may be targets for developing drugs for HD.

Giving Huntington's disease the finger? Two teams report success for zinc-finger drugs in cells and mice

Giving Huntington's disease the finger? Two teams report success for zinc-finger drugs in cells and mice

Dr Ed Wild on November 01, 2012

Designing drugs that tell our cells to make less of the harmful mutant huntingtin protein is one of the most promising approaches to treating Huntington's disease. Most huntingtin-lowering attempts so far have tried to 'shoot the messenger' rather than attacking the source of the message - the DNA itself. Now, two independent reports of success in HD mice have given a boost to 'zinc finger' drugs - which interact directly with the HD gene itself. It's early days for this new technology: what do we know, and what challenges are ahead?

Interview: Alice and Nancy Wexler

Interview: Alice and Nancy Wexler

Dr Ed Wild on October 20, 2012

The Hereditary Disease Foundation, or HDF, is a key player in the world of Huntington's disease research. At the HDF's recent biennial scientific meeting in Cambridge, Massachusetts - 'The Milton Wexler Celebration of Life and Creativity' - HDBuzz met Nancy and Alice Wexler, the remarkable sisters at the heart of the HDF's work.

Video: What’s new in Huntington's disease research 2012

Video: What’s new in Huntington's disease research 2012

Dr Ed Wild on October 10, 2012

Watch the video of Ed Wild's address to the European Huntington's Association annual meeting in September 2012, summarizing how therapies research works and explaining the most exciting ways researchers are trying to study and treat HD.

Shooting the messenger with single-stranded RNA gene silencing

Shooting the messenger with single-stranded RNA gene silencing

Dr Nayana Lahiri on September 24, 2012

After huge leaps forward in recent years, we're edging ever closer to human trials of huntingtin lowering or 'gene silencing' as a potential treatment for Huntington’s Disease. Newer, better and safer techniques are always welcome and the announcement of ‘single-stranded RNA’ silencing is causing quite a hubbub. What’s it all about?

EuroBuzz Video: Day 2

EuroBuzz Video: Day 2

Dr Jeff Carroll on September 21, 2012

Jeff Carroll and Ed Wild present EuroBuzz episode 2 - bringing the European HD Network Meeting direct to you, in plain language. Watch online!

EuroBuzz News: Day 2

EuroBuzz News: Day 2

Dr Ed Wild on September 15, 2012

Our second daily report from the European Huntington’s Disease Network 2012 Meeting in Stockholm. Video of both EuroBuzz evening sessions will be available to watch on HDBuzz.net next week.

ASO gene silencing reaches further, lasts longer

ASO gene silencing reaches further, lasts longer

Dr Nayana Lahiri on June 21, 2012

Drugs called anti-sense oligonucleotides, or ASOs, are one way of silencing the gene that causes Huntington's disease. A new publication in the journal Neuron suggests that ASO gene silencing reaches further in the brain than other methods, lasts longer and is safe.

Mutant yeast highlights crucial CAG-reading protein

Mutant yeast highlights crucial CAG-reading protein

Dr Ed Wild on March 14, 2012

A study in yeast has highlighted a DNA-reading protein called SPT4 as possibly controlling which CAG-containing genes are active. Since Huntington's disease is caused by a gene with a long CAG stretch, this might be important for understanding how the HD gene works.