Felodipine is a medication of the calcium channel blocker type which is used to treat high blood pressure.
In a recent study from the University of Cambridge, researchers found that felodipine may help treat Huntington’s, Parkinson’s disease, and dementia.
Previous research has shown that Huntington’s, Parkinson’s, and dementia have a common feature: The build-up of misfolded proteins.
In Huntington’s disease, the protein is huntingtin, and in some dementias, the protein is tau. These proteins can form ‘aggregates’ that lead to irreversible damage to nerve cells in the brain.
In healthy people, the body uses a mechanism called autophagy, or ‘self-eating’, to prevent the build-up of misfolded proteins.
The mechanism could eat cells and break down the materials. However, in the diseases, the mechanism is impaired and the brain cannot clear the proteins building up.
Currently, there are no drugs that can induce autophagy effectively in patients.
In the study, the team showed that the drug could help induce autophagy in several neurodegenerative diseases.
The drug was effective to reduce in mice with Huntington’s and Parkinson’s disease mutations. In addition, it reduced the build-up of aggregates in zebra with dementia.
This is the first time a study has shown that an approved drug can slow the build-up of harmful proteins in the brain. Future research needs to test the drug’s effect on humans.
The findings show that re-purposing existing drugs has the advantage that the drugs have already been shown to be safe for use in humans.
If this blood pressure drug can be shown to be effective against the target diseases in humans, then the journey to clinical use can be much faster.
If you care about dementia, please read studies about a new way to treat dementia and Vitamin B supplements could help reduce dementia risk.
For more information about dementia, please see recent studies about antioxidants that could help reduce dementia risk, and Vitamin D deficiency linked to higher dementia risk.
The finding was published in the journal Nature Communications and conducted by Professor David Rubinsztein et al.
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