NWPF

News ArchivesRead News

New discovery offers hope for Parkinson's

Saturday May 11, 2013

Times of India - Scientists have discovered the three-dimensional structure of the protein Parkin, a finding which may provide new ways to develop drugs to slow the progression of Parkinson's disease.

Researchers from McGill University worked in collaboration with teams led by Dr Edward A Fon at the Montreal Neurological Institute and Hospital - The Neuro, and Dr Kalle Gehring in the Department of Biochemistry at the Faculty of Medicine.

Mutations in Parkin cause a rare hereditary form of Parkinson's disease and are likely to also be involved in more commonly occurring forms of Parkinson's disease.

The Parkin protein protects neurons from cell death due to an accumulation of defective mitochondria. Mitochondria are the batteries in cells, providing the power for cell functions.

This new knowledge of Parkin's structure has allowed the scientists to design mutations in Parkin that make it better at recognising damaged mitochondria and therefore possibly provide better protection for nerve cells.

"The majority of Parkinson's patients suffer from a sporadic form of the disease that occurs from a complex interplay of genetic and environmental factors which are still not fully understood," said Fon, neurologist at The Neuro and head of the McGill Parkinson Programme.

"A minority of patients have genetic mutations in genes such as Parkin that cause the disease. Although there are differences between the genetic and sporadic forms, there is good reason to believe that understanding one will inform us about the other.

"It's known that toxins that poison mitochondria can lead to Parkinson's-like symptoms in humans and animals. Recently, Parkin was shown to be a key player in the cell's system for identifying and removing damaged mitochondria," Fon said.

Gehring likens Parkin to a watchdog for damaged mitochondria.

"Our structural studies show that Parkin is normally kept in check by a part of the protein that acts as a leash to restrict Parkin activity. When we made mutations in this specific 'leash' region in the protein, we found that Parkin recognised damaged mitochondria more quickly," Gehring said.

"If we can reproduce this response with a drug rather than mutations, we might be able to slow the progression of disease in Parkinson's patients," Gehring added.

The research will be published in the journal Science.

Recent News

May 20 - Book Review: Aging in the Key of Humor
May 19 - Press Release: The Michael J. Fox Foundation for Parkinson's Research Joins Multinational Critical Path for Parkinson's Consortium
May 19 - Congress reaches deal to overhaul chemical regulation
May 16 - Lifestyle: Why Parkinson's disease won't stop me rowing across the Pacific
May 16 - Many biomarkers for PD fail to inform on progression
May 10 - Parkinson's Cell Transplant Shows Good Reinnervation at 24 Years
May 7 - Growing art installation gathers stories of living with Parkinson's
May 5 - New technique can provide better cell transplants against Parkinson's disease
May 2 - What's Good For The Heart Is Good For The Brain
Apr 29 - Press Release: FDA approves first drug to treat hallucinations and delusions associated with Parkinson’s disease
Apr 28 - Dopamine-making neurons can be chemically controlled in animal model of Parkinson's
Apr 25 - Lifestyle: Dating with Disease
Apr 25 - Scientific breakthrough in fight against Parkinson's and Alzheimer's
Apr 20 - Breakthrough Parkinson's disease blood test
Apr 15 - Living with Parkinson's
Apr 12 - Tissue biomarker for dementia with Lewy bodies and Parkinson’s disease
Apr 11 - Yoga for Every Body: Experts say yoga can ease pain and improve mobility for people with neurologic conditions
Apr 9 - Commonly prescribed Parkinson's drugs up risk of compulsive gambling, shopping, binge eating, hypersexuality
Apr 7 - Pfizer and IBM Launch Innovative Research Project to Transform Parkinson's Disease Care
Apr 7 - Parkinson's Drug Highly Effective for Resistant Depression