Prozac helps learning and memory in people with Huntington's disease

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Howard Florey Institute scientists in Melbourne have found that fluoxetine (commonly marketed as Prozac) not only improves depression in Huntington's disease, but also improves learning and memory.

Dr Anthony Hannan and his team also found that fluoxetine restores the brain's process of neurogenesis - the birth of new neurons - to normal levels, which helps delay the onset of the inherited fatal disease.

People with Huntington's disease have progressive motor problems, cognitive deficits (dementia) and psychiatric symptoms (the most common is depression) that usually start to appear in mid-life. There is no cure and death usually results within 10 to 20 years of symptom onset, or faster in the childhood-onset form of the disease. The disease is caused by a mutation in a single gene and when this defective gene is passed from parent to child, 50 percent of the offspring will inherit the disorder, which can be detected by genetic testing.

Dr Hannan said this discovery was an important step in developing effective treatments to delay the onset of symptoms and the progression of Huntington's disease.

"Now that we've found fluoxetine improves memory problems, or dementia, as well as depression in mice with Huntington's disease, further research can be conducted to see if the drug has the same benefits in humans with the disease," Dr Hannan said.

"We have started discussing arrangements with colleagues to begin human trials to see if fluoxetine, and related drugs, are also effective treatments in people with the disease."

"Fluoxetine's ability to promote the birth of new neurons in the normal and Huntington's brain provides new insight into the biological basis of depression, as well as other brain disorders involving dementia. It also suggests new applications for these antidepressant drugs," he said.

During the study, mice with the Huntington's gene and control mice were treated daily with either fluoxetine or saline. The mice were given cognitive tests to perform to determine the behavioural effects of the drug.

The scientists expected fluoxetine to improve the depressive-like symptoms, which they have shown for the first time in mice with Huntington's disease, but were surprised that it also improved cognitive symptoms.

Dr Hannan's findings will soon be published in the European Journal of Neuroscience.

Dr Hannan is internationally recognised for his research that proves mental and physical exercise can delay the onset of some degenerative brain disorders, including Huntington's disease. Brain disorders that were previously thought to be 100 percent genetic can actually be delayed, which brings great hope to sufferers of Huntington's disease.

Recent studies by Dr Hannan's group have also shown that mice with Huntington's disease actually display cognitive problems before the disease's typical movement problems appear. These results were recently been published in the Journal of Neuroscience. He has also shown that in Huntington's diseased brains, information processing between neurons is disrupted, but the neurons do not die, which means the brain may respond to new anti-dementia drugs that can restore memory.

Dr Hannan has just returned from Austria where he gave a special lecture on these findings and was presented with the Young Scientist Lecturer Award from the International Society of Neurochemistry. He also recently won two Australian Museum Eureka Prizes; the British Council Eureka Prize for Inspiring Science, as well as the inaugural Eureka People's Choice Award.

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