Saturday December 14, 2019

Parkinson Treatment Possible Through A Blood Pressure Drug

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. 

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blood pressure
"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. Pixabay

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.

drug

The hypertension drug was able to slow down progression of these potentially devastating conditions and “so we believe it should be trialled in patients,” he added. VOA

These proteins, such as huntingtin in Huntington’s disease and tau in some dementias, 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 trialled in patients,” he added.

brain

These proteins, such as huntingtin in Huntington’s disease and tau in some dementias, form “aggregates” that can cause irreversible damage to nerve cells in the brain.
Pixabay

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

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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. (IANS)

Next Story

This Protein in the Human Brain Can Protect Against Alzheimer’s disease

Brain protein that could protect against Alzheimer's disease

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Human Brain
Immune cells in the brain, called microglia, play a critical role in Alzheimer's disease. Pixabay

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results published in the journal Communications Biology suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained study co-author Matthew Macauley, Assistant Professor at University of Alberta in Edmonton, Canada.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” Macauley added.

Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of Alzheimer’s disease.

Brain
CD33 protein in the brain plays a crucial role in modulating the function of microglia. Pixabay

Now, Macauley’s research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia.

“The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said Abhishek Bhattacherjee, first author and postdoctoral fellow in the Macauley lab.

Alzheimer’s disease affects more than 44 million people around the world.

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“These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said Macauley.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse Alzheimer’s disease can be envisioned,” Macauley said. (IANS)