In studies carried out on mice and zebrafish, a prescribed drug for hypertension may be promising for treating a collection of neurodegenerative diseases. Neurodegenerative diseases are a result of a build-up of misfolded proteins that cause 'aggregates' and result in irreversible damage to the nerve cells in the brain.
For healthy individuals, a build-up of proteins is resolved by autophagy--a mechanism used by the body that involves 'Pac-Man'-like cells that eradicate toxic materials. However, in neurodegenerative diseases, autophagy is impaired and thus, cannot clear the protein build-up in the brain.
The need to develop drugs that can induce autophagy effectively in neurodegenerative patients has been increasingly critical than ever. Such urgency has pushed scientists to look into re-purposing existing drugs. Drug re-purposing holds the advantage of having already been shown to be safe for use in humans which makes the process of clinical use much faster in the treatment of other targeted diseases.
Now, in a study published in Nature Communications, felodipine, a drug for the treatment of hypertension, may serve as a candidate for re-purposing in the treatment of neurodegenerative diseases. Specifically, felodipine has been shown to induce autophagy and could alleviate the symptoms of neurodegenerative disease.
In mice and zebrafish, felodipine was effective at decreasing the build-up of toxic aggregates in diseases like Huntington, Parkinson and dementia models.
"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," says Professor David Rubinsztein. "As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialled in patients."
"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."
Source: University of Cambridge
