BP drug shows promise for treating Parkinson's
Felodipine, a prescribed drug to treat high blood pressure, has shown promise against Parkinson's, Huntington's and forms of dementia in studies carried out in mice and zebrafish at the University of Cambridge.
In a study published in the journal Nature Communications, scientists have shown in mice that felodipine may be a candidate for re-purposing. A common feature of neurodegenerative diseases is the build-up of misfolded proteins.
These proteins, such as huntingtin in Huntington's disease and tau in some dementia, form "aggregates" that can cause irreversible damage to nerve cells in the brain.
A team led by Professor David Rubinsztein used mice that had been genetically modified to express mutations that cause Huntington's disease or a form of Parkinson's disease, and zebrafish that model a form of dementia.
Felodipine was effective at reducing the build-up of "aggregates" in mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases.
"This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," said Professor Rubinsztein
The hypertension drug was able to slow down progression of these potentially devastating conditions and "so we believe it should be trialed in patients," he added.
In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials. This mechanism is known as autophagy, or 'self-eating', and involves cells eating and breaking down the materials.
"This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic," said Professor Rubinsztein.
In a study published in the journal Nature Communications, scientists have shown in mice that felodipine may be a candidate for re-purposing. A common feature of neurodegenerative diseases is the build-up of misfolded proteins.
These proteins, such as huntingtin in Huntington's disease and tau in some dementia, form "aggregates" that can cause irreversible damage to nerve cells in the brain.
A team led by Professor David Rubinsztein used mice that had been genetically modified to express mutations that cause Huntington's disease or a form of Parkinson's disease, and zebrafish that model a form of dementia.
Felodipine was effective at reducing the build-up of "aggregates" in mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases.
"This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," said Professor Rubinsztein
The hypertension drug was able to slow down progression of these potentially devastating conditions and "so we believe it should be trialed in patients," he added.
In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials. This mechanism is known as autophagy, or 'self-eating', and involves cells eating and breaking down the materials.
"This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic," said Professor Rubinsztein.