How ‘shredder’ gene could shield against Alzheimer’s disease
ALZHEIMER’S disease could be prevented before it starts using a gene which shreds protein tangles in the brain.
Researchers at Glasgow University discovered the ‘protein clumps’ which cause degenerative conditions such as Alzheimer’s and Parkinson’s disease are pulled apart by a single gene, which activates this action within brain cells.
Then it ‘instructs’ the cells to shred these clumps to stop them tangling up once again.
The gene, UBQLN2, was seen to trigger these two important processes in mice, and did not do so when it mutated or developed a fault.
It suggests if scientists found a way to stimulate this gene artificially, they could stop protein clumping, which happens naturally as we age, before it causes us to fall ill.
The study, published in the journal Cell, was led by Dr Thimo Kurz at the University of Glasgow, who said: ‘We are excited about this, as it could lead to a stimulation of the gene which could rid the body of these [protein] plaques.
‘This could help alleviate symptoms in sufferers, or even prevent the proteins from forming in people if we identified those at risk first.’
Protein clumps are known to help trigger not only dementia, but Huntington’s disease – an incurable condition that causes tremors, personality change and mobility problems.
They also lead to Parkinson’s, the condition suffered by comedian Billy Connolly, which also causes tremors and can lead to severe memory loss.
People with Parkinson’s do not have enough dopamine, a crucial chemical in the brain, produced by vital cells which protein clumps attack.
Researchers looking at the UBQLN2 gene found its main function is to help cells remove these dangerous tangles and put them through a cellular shredder prevent them clumping again. Previous work has shown when the gene is faulty, it leads to motor neurone disease and dementia, although it was not fully understood why.
Now scientists understand exactly how UBQLN2 works, they will work to harness it for patients’ benefit.
Research assistant Dr Roland Hjerpe said: ‘[The study] has implications for most neurodegenerative diseases and can open up avenues for new therapeutic interventions to treat these conditions in the future.’
Clare Bale, from charity Parkinson’s UK, said last night: ‘This is a crucial route to potential new therapies that have the power to slow or stop the development of Parkinson’s – something no current treatment can do.’
But the Alzheimer’s Society was more cautious, saying further research was needed.
Research officer Dr Louise Walker said: ‘We do not know for sure whether this gene is directly involved in the development of Alzheimer’s.’
‘Help alleviate symptoms’