To treat high blood pressure may now become possible through a prescribed drug that has shown promise against diseases like Huntington's Parkinson's and forms of dementia in studies carried out in zebrafish and mice at the University of Cambridge.
Collectively known as neurodegenerative diseases, a typical feature of these diseases is the build-up of misfolded proteins. These proteins including Huntington's disease and tau in some dementia, form "aggregates" that is capable of causing irreversible damage to nerve cells in the brain.
The body of a healthy person uses a mechanism to prevent the build-up of such toxic materials. This prevention mechanism is called autophagy, or "self-eating," and involves "Pac-Man" - like cells eating and breaking down the contents. In neurodegenerative diseases, however, this mechanism is impaired and unable to clear the proteins building up in the brain.
With the age of the global population, an increasing number of individuals are being diagnosed with neurodegenerative diseases, and this makes it the search for effective drugs ever more urgent. Currently, there are no drugs to induce autophagy effectively in patients.
Added to the searching for new drugs, scientists often look for re-purpose existing drugs. These systems have the advantage that they have already been shown to be safe for use in humans. If these drugs can be shown to be effective against the target diseases, then the journey to clinical application is much faster.
Scientists at the UK Dementia Research Institute and the Cambridge Institute for Medical Research at the University of Cambridge published a study in the journal Nature Communications that have shown in mice that felodipine, a hypertension drug, might be a candidate for re-purposing.
In the epidemiological studies, there was a hint of a possible connection between the drug and reduced risk of Parking's disease, but now the researchers have shown that it may be able to induce autophagy in several neurodegenerative conditions.
Professor David Rubinsztein led a team that used mice that had been genetically modified to express mutations that caused Huntington's disease or a form of Parkinson's disease and zebrafish that model a form of dementia.
Professor Rubinsztein said that this is the first time that they are aware of a study that has shown that an approved drug can slow the build-up of toxic proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans. Consequently, the drug was able to slow down the progression of these potentially devastating conditions and so the researchers believe it should be trialed in patients.
He concluded that this is only the first stage and the drug needs to be tested in patients to see if it has the same effects in humans as it does in mice. He emphasized on the need for scientists to be cautious, but he believes that they can be cautiously optimistic.
