ONE gene could protect against degenerative Alzheimer’s and Parkinson’s disease

Aug. 2, 2016

A SINGLE gene could protect against the causes of neurodegenerative diseases including Alzheimer’s, Parkinson’s and Huntington’s disease.

One gene could protect against neurodegenerative disorders

Research, led by the University of Glasgow, has identified how cells protect themselves against ‘protein clumps’ known to be the cause of the devastating conditions.

The study, which is published today in Cell and was conducted in collaboration with the MRC Protein Phosphorylation and Ubiquitylation Unit at the University of Dundee.

It offers an insight into the role of a gene called UBQLN2 and how it helps to remove toxic protein clumps from the body and protect it from disease.

Using biochemistry, cell biology and sophisticated mouse models, the researchers discovered that the main function of UBQLN2 is to help the cell to remove dangerous protein clumps – a role which it performs by first detangling clumps, then shredding them to prevent future tangles.

Parkinson's is also a neurodegenerative disorder

Protein clumps occur as part of the natural ageing process, but are normally detangled and disposed of as a result of the gene UBQLN2. 

However when this gene mutates, or becomes faulty, it can no longer help the cell to remove these toxic protein clumps, which leads to neurodegenerative disease.

Dr Thimo Kurz, from the Institute of Molecular, Cell and Systems Biology, said: “The function of UBQNL2 is connected to many neurodegenerative disorders, such as Parkinson’s, Alzheimer’s and Huntington’s disease.

“These patients often have very clear clumps in their brain cells. 

Using mice that mimic human Huntington’s disease, we found that when UBQLN2 is mutated, it could no longer help nerve cells to remove protein clumps in the brains of these mice.”

One gene could cause the progressive illnesses

Previous work has shown that when the UBQLN2 gene is faulty, it leads to a neurodegenerative disease called Amyotrophic Lateral Sclerosis with Frontotemporal Dementia (ALS/FTD or motor-neuron disease with dementia). 

Until this study it was not fully understood why mutation of this gene caused disease.
 
Now that scientists understand exactly how UBQLN2 works and what it does and why its mutation appears to be so detrimental to the body.

They said they hope their findings will pave the way for new research into novel treatment options for patients with neurodegenerative diseases.

Dr Roland Hjerpe said: “The significance of this discovery goes beyond the role of UBQLN2 in motor-neuron disease with dementia.

“Our study has revealed a new mechanism by which nerve cells cope with protein clumps in general, which has implications for most neurodegenerative diseases and can open up avenues for new therapeutic interventions to treat these conditions in the future."                                                                     
The study ‘UBQLN2 connects the proteasome with the HSP70 system to promote autophagy-independent protein aggregate clearance’ is published in Cell. 

Alzheimer’s disease is the most common cause of dementia, affecting an estimated 500,000 people in the UK - but not all dementia is Alzheimer’s disease.

Care home

Other types of dementia include vascular dementia and mixed dementia.

Cases of dementia can be caused by other illnesses such as strokes.

Dementia is a set of symptoms which can include memory loss, difficulty problem solving, thinking and can lead to behavioural changes such as a change in temperament or mood but it can affect people in very different ways. 

Parkinson’s occurs when nerve cells in the brain die and causes sufferers problems with mobility, speech and often mental health.

Video:

http://www.express.co.uk/life-style/health/695698/One-gene-protect-against-Alzheimers-Parkinsons-Huntingtons

http://www.express.co.uk/life-style/health/695698/One-gene-protect-against-Alzheimers-Parkinsons-Huntingtons