Our final daily report from the Huntington’s disease World Congress brings together all the live updates from our twitter feed. Video of both Oz Buzz sessions – with news, interviews and features – is on YouTube now and will be available to watch at HDBuzz.net later this week.
Wednesday, September 14, 2011
8:33 – Jeff and Ed are now live from day 3 of the World Congress on HD!
8:40 – Jeff: HD may be much more common than we thought – Michael Hayden
8:47 – Jeff: HD is an increasing burden on the elderly, who in the past may not have lived long enough to have symptoms – Hayden
9:02 – Ed: More on increased ‘prevalence’ of HD – how it’s more common than we thought
9:07 – Ed: studies in sperm helping to predict whether a CAG repeat in the ‘gray area’ will cause problems for next generation
9:13 – We need to move away from talking about ‘onset’ in Huntington’s – symptoms begin gradually over years – Dr Mark Guttman
9:32 – Huntington’s disease causes a wide variety of symptoms so doctors should always bear it in mind when seeing patients- Elizabeth McKusker
10:36 – Ed’s reporting from the ‘Science: omics’ session – Jeff’s in ‘International models of care’.
10:37 – Ed: ‘omics’ means measuring loads of things at once. Like genomics (looking at tons of genes)
10:45 – Ed: Metabolomics is measuring metabolites – small molecules in blood. Wayne Matson’s done it in HD & finds interesting changes
10:54 – Ed: Levels of a chemical I3PA seem to be reduced in blood of HD patients and HD mice. Not yet clear why but could be useful – Matson
11:02 – Jeff: HD patient care in Australia is difficult because of complex health care administration – Andrew Churchyard
11:00 – Jeff: Significant numbers of HD families don’t interact with the medical system, and we don’t know why – Churchyard
11:11 – Ed: Brain immune cells called microglia are abnormal in HD mice – Dr Blair Leavitt – are they helping or harming?
11:13 – Ed: There are also changes in the mice’s brain blood vessels that could increase the cross-talk between brain & body – Leavitt
11:26 – Jeff: Access to medical services for HD families in South Africa is limited – Amanda Krause
11:34 – Jeff: In black Africans a disease called ‘HD like 2’ looks very much like HD, but is caused by a different mutation – Krause
11:38 – Ed: Ruth Luthi-Carter examines which genes are more and less activated in different mouse models of HD & compares them to humans
11:51 – Ed: These gene activation changes could help us to understand the disease and develop and test new drugs – Luthi-Carter
12:06 – Ed: Proteins do stuff by sticking to each other. Mutant and normal huntingtin stick to different groups of partners – Chris Ross
12:11 – Ed: An international consortium of researchers is using stem cell models to help understand Huntington’s disease
12:18 – Jeff: Francisco Cardoso – new Latin american HD network active at rlah.org
12:20 – Ed: The consortium has figured out the recipe for turning stem cells into the neurons most affected by HD. Very valuable research tool
12:27 – Red Latino-Americana de Huntington: investigación de tratamientos efectivos para la Enfermedad de Huntington
12:43 – Ed: Comparing gene switching and behavior across mouse models shows that different models mimic different aspects of HD Lesley Jones
12:44 – Ed: One of the mouse models called Q150 actually produces less huntingtin protein overall – weird but important to know about – Jones
12:45 – Ed: An HDBuzz article on the different mice used in Huntington’s disease research is coming soon
13:47 – Ed and Jeff are now reporting from the final science session – late breaking hot topics. Jeff is the first speaker in the session!
13:56 – Jeff studies metabolites in several tissues in HD mice. Tissues like brain, fat and liver are all changed differently by the mutation.
14:00 – Metabolic changes Jeff found in HD mouse blood mirror the changes in the brain – could be useful for studying human patients
14:19 – Dimebon showed no benefit for HD in big trial- HORIZON. The quest for treatments for thinking probs continues.
14:21 – However, HORIZON study recruited rapidly and was run efficiently – good news for future trials of upcoming treatments – Bernhard Landwehrmeyer
14:42 – Chemical ‘tattoos’ are added to DNA by enzymes. HD messes this up. HDAC inhibitor drugs should help – a trial’s underway – Larry Marsh
14:50 – There are many different DNA ‘tattoos’ = many ways to try to improve things with drugs. Animal studies will identify best ones – Marsh
15:10 – Jeff: Clare van Eyk uses fruit flies to try and understand how the mutated huntingtin gene kills brain cells
15:12 – ‘RNA’, as well as protein might contribute to brain cells dying – Clare
15:13 – Jennifer Thompson is studying the psychiatric symptoms of HD, like apathy and depression, which can be devastating
15:16 – Apathy is incredibly common in HD, and worsens over time – Thompson
15:18 – Interestingly, depression is also common in HD, but doesn’t seem to change much over time – Thompson
15:36 – Robi Blumenstein of CHDI – like a chess game, we need to think far ahead if we’re going to beat Huntington’s disease
15:40 – Success is a three-legged stool: (1) an effective treatment (2) the ability to test it and (3) enough trial volunteers – Blumenstein
16:00 – Lots of HD family members needed for trials, now & future. Find out how to get involved at Enroll-HD.org
