Ancestry plays a role in MND risk genes

21 Nov 2017

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MND risk genes ancestry

Your ancestry can impact the risk of developing motor neurone disease (MND), new research shows.

The collaborative international study, involving Professor Naomi Wray from UQ’s Institute for Molecular Bioscience (IMB) and QBI, has identified a gene associated with MND (also known as Amyotrophic lateral sclerosis - ALS) in people of Chinese ancestry.

MND is a rapidly progressing neurological disorder that attacks the nerve cells in the brain and spinal cord controlling the way we walk, talk, eat, speak, and breathe. The loss of these nerve cells leads to progressive muscle weakness and wasting, and on average people live only about 2.5 years after the disease onset.

“Most research to date has focused on people of European ancestry, and last year, a gene called NEK1 was identified as being important in the disease onset for some people,” said Professor Wray.

“In this study, we have shown that NEK1 also contributes to disease in some Chinese people who have MND. Verification of the importance of this gene in a different ancestry will help prioritise molecular investigations of the role this gene plays in MND,” she said.

Clues to risk of developing sporadic MND

The team focused on the most common form of MND, known as sporadic MND.

Most MND research focuses on the strongly familial form of MND, but more than 90 per cent of people with the disease have no family history of MND and their onset is sudden and unexpected.

Recently, Professor’s Wray’s research identified a location on the genome that’s associated with non-inherited MND.

Key collaborators included Professor Matthew Brown from the Queensland University of Technology’s Institute of Health and Biomedical Innovation, and Professor Dongsheng Fan of Peking University Third Hospital, Beijing. 

The research was made possible with the generous support of organisations and individuals, especially the Peter Goodenough bequest, the Motor Neurone Disease Research Institute of Australia, and the Ross Maclean Senior Research Fellowship.

Other supporting organisations include the Australian Research Council and the National Health and Medical Research Council.

The study is published in Genome Medicine.

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