Huntington’s disease research news. In plain language. Written by scientists. For the global HD community.
Researchers have developed a new technique that allows them to screen for genes that could contribute to the progression of Huntington’s disease and other neurodegenerative disorders. This is the first time this is possible in the mammalian central nervous system. They used the technique in an HD mouse to uncover an antioxidant gene, Gpx6, which is protective to neurons.
Most research on Huntington’s disease is done using animal models that mimic the human disease. However, these models typically recreate only a few of the disease’s symptoms, and there are some important symptoms that don’t show up in any model at all. Now, exciting new research is making great strides against these problems – and teaching us about the disease at the same time.
A recent study by the Yang lab at UCLA points to a new idea for preventing damage to neurons in Huntington’s disease. The strategy is to tone down an overly helpful protein called ATM. Inside neurons, ATM provides a crucial role in repairing the cell’s infrastructure, somewhat like that of a bridge inspector, but the expanded HD protein may be causing ATM to misjudge DNA damage.
Our final report from the Annual Huntington's Disease Therapeutics Conference.
Our second update from the Annual Huntington's Disease Therapeutics Conference.
The first of our special reports from the Annual Huntington's Disease Therapeutics Conference in Palm Springs – the biggest meeting of HD scientists focused on developing treatments to prevent or slow Huntington's disease.
The growth factor 'BDNF' usually sends a “Survive!” signal to brain cells. In Huntington’s Disease (HD), this system doesn’t work as it should, so scientists have been looking for ways to boost the signal. Enter one of nature’s most useful tools: the antibody. Usually antibodies play an important role in the immune system, but researchers have identified two antibodies, produced by the company Pfizer, that can act like a set of spare keys to activate the TrkB receptor. This unlocks the door to determining whether a boost in TrkB activity is enough to prevent neurons from dying, in hopes of slowing the progression of HD.
In Huntington’s Disease, one of the many problems arising from the disease mutation is that DNA gets folded incorrectly. A new study in mice reveals that a drug changing the way DNA folds may have beneficial effects in Huntington’s – even for the untreated offspring of treated individuals. This discovery could affect how we think about drug therapies for Huntington’s Disease.
What happens when you have a broken part in a machine? You fix it! A new study shows that increasing the activity a critical piece of machinery called ‘mTORC1’ in a mouse model of Huntington’s disease leads to improved motor problems and brain abnormalities associated with the disease. These recently published findings may offer scientists a new target for therapeutic development in HD.