Wednesday July 18, 2018

New Target For Parkinson’s Therapy Identified

The study revealed that, inside cells, alpha-synuclein binds to mitochondria, where cardiolipin resides

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The reason that Parkinson’s disease develops is not known. Wikimedia commons
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Researchers have discovered one of the factors behind nerve cell death in Parkinson’s disease, unlocking the potential for new treatment to slow the progression of this fatal neurodegenerative disorder.

The researchers found that cardiolipin — a molecule inside nerve cells — helps ensure that a protein called alpha-synuclein folds properly. Misfolding of this protein leads to protein deposits that are the hallmark of Parkinson’s disease.

“Identifying the crucial role cardiolipin plays in keeping these proteins functional means cardiolipin may represent a new target for the development of therapies against Parkinson’s disease,” said Scott Ryan, Professor at the University of Guelph in Ontario, Canada.

“Currently there are no treatments that stop nerve cells from dying,” Ryan added.

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These deposits are toxic to nerve cells that control voluntary movement. When too many of these deposits accumulate, nerve cells die, the researchers said.

For the study, published in the journal Nature Communications, researchers used stem cells collected from people with the disease. The team studied how nerve cells try to cope with misfolded alpha-synuclein.

10 million people living worldwide suffer from Parkinson;s disease Pixabay
10 million people living worldwide suffer from Parkinson’s disease. Pixabay

“We thought if we can better understand how cells normally fold alpha-synuclein, we may be able to exploit that process to dissolve these aggregates and slow the spread of the disease,” Ryan said.

The study revealed that, inside cells, alpha-synuclein binds to mitochondria, where cardiolipin resides. Cells use mitochondria to generate energy and drive metabolism.

ALSO READ: Progression of Parkinson disease could be slowed with exercise

Normally, cardiolipin in mitochondria pulls synuclein out of toxic protein deposits and refolds it into a non-toxic shape, the researchers added.

The researchers found that, in people with Parkinson’s disease, this process is overwhelmed over time and mitochondria are ultimately destroyed.

“As a result, the cells slowly die. Based on this finding, we now have a better understanding of why nerve cells die in Parkinson’s disease and how we might be able to intervene,” the researchers noted. (IANS)

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Study: Experimental Drug can Halt Parkinson’s Progression

The drug, named NLY01, is similar to compounds used to treat diabetes and is expected to move to clinical trials this year

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Study: Experimental Drug can Halt Parkinson's Progression
Study: Experimental Drug can Halt Parkinson's Progression. Pixabay

US researchers have developed an experimental drug that potentially slows down the progression of Parkinson’s disease as well as its symptoms.

In experiments performed with cultures of human brain cells and live mouse models, researchers from the Johns Hopkins University in Maryland reported that the drug blocked the degradation of brain cells that is the hallmark of Parkinson’s disease.

“It is amazingly protective of target nerve cells,” said Ted Dawson, Professor at the University’s School of Medicine.

The drug, named NLY01, is similar to compounds used to treat diabetes and is expected to move to clinical trials this year.

If successful in humans, it could be one of the first treatments to directly target the progression of Parkinson’s, not just the muscle rigidity, spasmodic movements, fatigue, dizziness, dementia and other symptoms of the disorder, Dawson said in the paper published in the journal Nature Medicine.

Parkinsons
Representational image. (IANS)

In a preliminary experiment in laboratory-grown human brain cells, Dawson’s team treated human microglia — a brain cell type that sends signals throughout the central nervous system in response to infection or injury — with NLY01 and found that they were able to turn the activating signals off.

Further, the researchers injected the mice with alpha-synuclein — the protein known to be the primary driver of Parkinson’s disease — and the mice treated with NLY01 maintained normal physical function and had no loss of dopamine neurons, indicating that the drug protected against the development of Parkinson’s disease.

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In another experiment, the team used mice that were genetically engineered to naturally produce more human-type alpha-synuclein typically used to model human Parkinson’s disease that runs in families.

While under normal conditions, these so-called transgenic mice will succumb to the disease in 387 days, those treated with NLY01 extended the lives by over 120 days.

However, the experimental drug must still be tested for safety as well as effectiveness in people, Dawson cautioned. (IANS)