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The BP drug shows the promise to treat Parkinson's

Be careful if you use sleep pills regularly, as a new study has shown that it can affect your blood pressure (BP) in older adults. Felodipine, a prescribed drug for treating high blood pressure, has shown promise to Parkinson's, Huntington's and forms of dementia in studies conducted in mice and zebrafish at the University of Cambridge. In a study published in the journal Nature Communications, researchers have shown in mice that felodipine may be a candidate for repositioning. A common feature of neurodegenerative diseases is the buildup of folded proteins. These proteins, such as huntingtin in Huntington's disease and rope in some dementia, form "aggregates" which can cause irreversible damage to neurons 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 which is a form of dementia. Felodipine was effective in reducing the build up of "aggregates" in mice with the mutations of Huntington's and Parkinson's disease and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases. "This is the first time we are aware that a study has shown that an approved drug can slow down the build-up of harmful proteins in the brains of mice with doses designed to mimic the concentration of the drug seen in humans," Professor Rubinsztein. The high blood pressure agent could delay the development of these potentially devastating conditions and "so we believe it…

Be careful if you use sleep pills regularly, as a new study has shown that it can affect your blood pressure (BP) in older adults.

Felodipine, a prescribed drug for treating high blood pressure, has shown promise to Parkinson’s, Huntington’s and forms of dementia in studies conducted in mice and zebrafish at the University of Cambridge.

In a study published in the journal Nature Communications, researchers have shown in mice that felodipine may be a candidate for repositioning. A common feature of neurodegenerative diseases is the buildup of folded proteins.

These proteins, such as huntingtin in Huntington’s disease and rope in some dementia, form “aggregates” which can cause irreversible damage to neurons 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 which is a form of dementia.

Felodipine was effective in reducing the build up of “aggregates” in mice with the mutations of Huntington’s and Parkinson’s disease and in the zebrafish dementia model.

The treated animals also showed fewer signs of the diseases.

“This is the first time we are aware that a study has shown that an approved drug can slow down the build-up of harmful proteins in the brains of mice with doses designed to mimic the concentration of the drug seen in humans,” Professor Rubinsztein.

The high blood pressure agent could delay the development of these potentially devastating conditions and “so we believe it should be tested in patients,” he added.

In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials.

This mechanism is called autophagy, or “self-eating,” and involves cells that eat and break down the materials.

“This is just the first step. The drug needs to be tested in the patients to see if it has the same effects in humans as in mice. We need to be careful, but I would say we can be cautiously optimistic,” says Professor Rubinsztein.


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