Epilepsy drug shows potential for Alzheimer's treatment

December 8, 2008

A drug commonly used to treat epilepsy could help clear the plaques in the brain associated with Alzheimer's disease, according to researchers at the University of Leeds. The plaques are known to lead to the progressive death of nerve cells in the brain linked to many forms of dementia.

Sodium valproate - which is marketed as the anti-seizure drug Epilim - has been shown by scientists at the University of Leeds to reactivate the body's own defences against a small protein called amyloid beta peptide, which is the main component of the brain plaques characteristic in Alzheimer's. Their work was funded by the Medical Research Council.

"The fact that we've been able to show that a well-established, safe and relatively inexpensive drug could help treat Alzheimer's is an extremely exciting development," says lead researcher Professor Tony Turner from the University's Faculty of Biological Sciences. "We hope colleagues will be able to progress this research with clinical trials in the near future."

Alzheimer's disease is the most common form of dementia and has no cure. In the UK today there a half a million people living with Alzheimer's – and this is likely to double within a generation unless new treatments are found.

Sodium valproate has been used for many years to suppress epileptic seizures and the many sufferers of epilepsy have been taking the drug for decades with few side effects.

The development of Alzheimer's is widely believed to be caused by the gradual accumulation in the brain of amyloid-beta peptide which is toxic to nerve cells. This is thought to be caused by a key enzyme called neprilysin or NEP gradually switching off in later life. One of NEP's roles is to clear the toxic peptide from the brain, and plaques begin to form as it gradually switches off, leading to the death of the brain's nerve cells.

The research team examined changes in chromatin – the 'packaging' that genes are contained within - and surmised that these changes might be involved in switching off NEP. The team found clear differences (acetylation) in key proteins within the chromatin when they compared normal nerve cells against those that failed to produce NEP.

"From there it was relatively simple to stimulate the expression of NEP with sodium valproate, which was seen to prevent the acetylation," says Professor Turner. "We were elated when we saw the results."

Source: University of Leeds

Explore further: New stem cell method produces millions of human brain and muscle cells in days

Related Stories

Insulin resistance may lead to faster cognitive decline

March 21, 2017

A new Tel Aviv University study published in the Journal of Alzheimer's Disease finds that insulin resistance, caused in part by obesity and physical inactivity, is also linked to a more rapid decline in cognitive performance. ...

Working towards a drug to limit brain injury

March 16, 2017

UNSW medical researchers in the Translational Neuroscience Facility are partnering with a drug development company to discover new treatments to limit the damage of traumatic brain injury.

Recommended for you

Opioid dependence can start in just a few days

March 16, 2017

(HealthDay)—Doctors who limit the supply of opioids they prescribe to three days or less may help patients avoid the dangers of dependence and addiction, a new study suggests.

1 comment

Adjust slider to filter visible comments by rank

Display comments: newest first

zecoseco
not rated yet Apr 29, 2009
good

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.