Proteome Systems and the High Q Foundation have announced the expansion of a biomarker discovery programme for Huntington's disease
The programme is seeking to discover biomarkers that will be used for monitoring the onset and progression of Huntington's disease (HD) and provide insights into the efficacy of existing and future treatments.
In the pilot programme commenced in April 2004, Proteome Systems identified changes in protein expression in a small set of Huntington's patients.
The expanded 18 month programme will apply proprietary targeted approaches to identify new biomarkers for the disease.
The intention is to develop clinical tests to assist in monitoring the onset and progression of the disease.
Proteome Systems will receive technology access fees and milestone payments under the 18 month programme, up to a maximum of US$3 million.
"We are delighted that the outcomes from the pilot programme have demonstrated our capacity to discover biomarkers for HD. "Our state of the art technology, combined with High Q's expertise and knowledge of HD, gives us a good chance of delivering tests that can assist in patient care and quality of life for HD sufferers" said Jenny Harry, head of discovery at Proteome Systems.
Allan Tobin, senior scientific advisor to the High Q Foundation, said "Proteome Systems has proven that its discovery researchers have made concrete progress on this HD biomarker programme.
"We are excited to expand the relationship with Proteome Systems and anticipate the discovery of biomarkers that will enable us to track the course and treatment of HD".
About Huntington's disease. Huntington's disease is an inherited genetic disease that affects approximately one in every 10,000 men and women and is invariably fatal.
Onset of the disease usually occurs between 30 and 50 years of age with deterioration of nerve cells that results in progressive motor, psychiatric and cognitive dysfunction, such as uncontrollable muscle movements, impaired thinking and depression.
The Huntington gene was mapped in 1983 and the mutation responsible for the disease discovered in 1993. Currently there are no effective treatments available to halt the development of the disease.
