Sunday March 24, 2019

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

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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Researchers To Develop Novel Therapy For Treating Parkinson’s Disease

Researchers developing new therapy to treat Parkinson's disease

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

Cell replacement may play an increasing role in alleviating the symptoms such as movement problems and memory loss of Parkinson’s disease (PD), researchers say.

The most common PD treatment today is based on enhancing the activity of the nigrostriatal pathway in the brain with dopamine-modulating therapies, thereby increasing striatal dopamine levels and improving motor impairment associated with the disease.

However, this treatment has significant long-term limitations and side effects.

“We are in desperate need of a better way of helping people with PD. It is on the increase worldwide. There is still no cure, and medications only go part way to fully treat incoordination and movement problems,” said Claire Henchcliffe, MD, from Weill Cornell Medicine in the US.

Parkinsons
Parkinson’s is caused by a lack of dopamine made by brain cells. (IANS)

Recent strides in stem cell technology mean that quality, consistency, activity, and safety can be assured, and that it is possible to grow essentially unlimited amounts of dopamine-producing nerve cells in the laboratory for transplantation, said a study, published in the Journal of Parkinson’s Disease.

“We are moving into a very exciting era for stem cell therapy. The first-generation cells are now being trialed and new advances in stem cell biology and genetic engineering promise even better cells and therapies in the future,” said Malin Parmar, postdoctoral candidate from the Lund University in Sweden.

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“There is a long road ahead in demonstrating how well stem cell-based reparative therapies will work, and much to understand about what, where, and how to deliver the cells, and to whom,” said Parmar. (IANS)