A CANCER drug has been found to help protect brain cells from the ravages of Alzheimer’s disease.
The discovery comes after scientists found that the toxic protein long thought to trigger dementia is not the real culprit.
Instead it is another protein entirely that sparks the destruction of vital brain connections.
The research paves the way for a treatment using the cancer drug nilotinib, which is already taken by patients to tackle a type of leukaemia.
When the culprit protein malfunctions it prevents cells clearing out a build-up of “rubbish” in the brain. Researchers at Georgetown University Medical Centre in Washington found nilotinib can help force the brain connections – called neurons – to clear the build-up.
The research, published online yesterday in the journal Molecular Neurodegeneration, found that neurons are killed when the tau protein, which was always known to play a role in the development of Alzheimer’s, fails to function.
Tau’s role is to provide a structure similar to a train track that allows the cells to clear accumulation of unwanted and toxic proteins.
Lead researcher Dr Charbel Moussa said: “When tau is abnormal, these proteins, which include amyloid beta, accumulate inside the neurons.
“The cells start to spit the proteins out as best they can so that they cannot exert their toxic effects inside the cell.
Understanding why nerve cells die in Alzheimer’s is a key goal in the search for treatments
“A drug that helps tau do its job may help protect against the disease progressing.”
The study suggests that it is the remaining amyloid beta protein – long thought to trigger dementia – that is not pushed out which destroys the cells, rather than the plaques that build up outside.
Dr Moussa added: “When tau does not function, the cell cannot remove the garbage, which at that point includes amyloid beta as well as tangles of non-functioning tau, and the cell dies.
“The amyloid beta released from the dead neuron then sticks to the plaque that had been forming.”
When tau was reintroduced into neurons that did not have it, plaque did not grow.
Malfunctioning tau can occur due to faulty genes or through ageing. As individuals grow older, some tau can malfunction while enough normal tau remains to help clear the garbage. In these cases, the neurons do not die.
Dr Moussa said: “That explains the confusing clinical observations of older people who have plaque build-up but no dementia.”
Tim Parry, of Alzheimer’s Research UK, said: “Understanding why nerve cells die in Alzheimer’s is a key goal in the search for treatments and this study adds to a body of evidence pointing to the tau protein as an important part of this process.”
In 2012 researchers in Cleveland, Ohio, found the skin cancer drug bexarotene could also help clear toxic plaque from the brain.