A potent anti-cancer drug may provide a new treatment for Alzheimer's disease, research suggests.
Protein clumps damage brain cell function
Tests on mice bred to develop Alzheimer's-like symptoms showed paclitaxel, known commercially as Paxceed, reduced signs of disease.
Researchers at the University of Pennsylvania showed the drug helps correct problems caused by the clumping of proteins in the nerve cells.
Details are published in Proceedings of the National Academy of Sciences.
The drug works by binding to and stabilising tiny structures inside cells called microtubules.
These structures play a key role in enabling brain cells to communicate effectively with each other.
A protein called tau helps keep them in good working order. However, this protein can sometimes become misshapened.
When this happens it can clump together inside cells, destroying their ability to communicate effectively and eventually kill them, causing symptoms of Alzheimer's and other neurodegenerative disorders.
Paclitaxel works by taking the place of tau, binding to the microtubules, and keeping them stable and in good working order.
The drug, along with other closely related variants, treats cancer by preventing cells from dividing. However, brain cells do not divide, and so this effect does not come into play when the drug is introduced into the brain.
In the latest study, mice were given weekly injections of paclitaxel.
It appeared to have a positive effect at both low and high doses.
Mice given the drug showed less signs of impaired movement than those who did not receive regular shots.
The researchers say that because drugs such as paclitaxel are already in use to treat cancer, it might be possible to set up clinical trials to test their effect on neurodegenerative diseases reasonably quickly.
However, they must find ways to ensure the drug can side step the body's defences and actually reach the brain.
Professor Simon Lovestone, chairman of the Scientific Advisory Board at the Alzheimer's Research Trust, "London research on fruit flies has suggested that, before neurons die in Alzheimer's disease, they lose their ability to send and carry signals.
"Finding a way to reverse these axonal transport problems before the cells die could offer a method of treating Alzheimer's disease before the symptoms become severe."
Professor Lovestone said the new research was exciting, particularly as the drug was already widely used, and therefore well understood pharmacologically.
"However, much more research is needed before we will know whether this could be developed into an effective treatment for Alzheimer's disease.
"We need to investigate further the toxicity the drug has been shown to have to neurons.
"Research will also be needed to see whether the beneficial effect will be reproduced in humans and to investigate the potentially unpleasant side-effects."