Dementia drug could be ‘within our grasp’, say Oz scientists
By ANIFriday, October 29, 2010
MELBOURNE - Australian scientists say that a drug treatment that could slow the onset of certain types of dementia could be ‘within our grasp’.
Dr John Kwok and colleagues from Neuroscience Research, Sydney, have identified a gene that causes abnormal protein deposits in the brains of people with frontotemporal dementia (FTD), a disease that affects people in their 50s and 60s.
Kwok said there were already several drugs approved for human use that were known to act on this gene.
“Common psychiatric drugs, such as haloperidol, used to treat schizophrenia, are known to act on this gene,” News.com.au quoted him as saying.
“Our hope is that these drugs will slow the progression of the disease,” he added.
Preliminary work with haloperidol suggested that a dose 10-100 times less than that used for treating psychosis could be effective.
“The exciting part about our findings is that an effective treatment for this form of dementia might be almost within our grasp,” Knok said.
“Because these drugs are already approved for use in humans, we could be looking at a treatment for frontotemporal dementia becoming available in just a few short years,” he added.
FTD is a type of dementia that affects personality, behaviour and language. Currently, there is no treatment to slow or stop this disease.
Like in Alzheimer’s disease, people with FTD develop unusual deposits of protein in their brains and the discovery of the gene responsible is a significant step.
By scanning DNA samples from a large Australian family with hereditary FTD, Knok identified the gene called SIGMAR1 responsible for the formation of these deposits. A further 26 families in Australia and 158 families in Europe were also screened.
“Identifying this gene gives us greater insight into how brain degeneration occurs in dementia,” he said.
Kwok is currently conducting tests in mice to see if haloperidol and other drugs can stop the abnormal build up of protein in the brain and prevent the death of brain cells in dementia.
The study was published in Annals of Neurology. (ANI)
