Gene that 'protects against Alzheimer's' could lead to 'new treatments for the disease'

Mail Online | 8/14/2019 | Alexandra Thompson Senior Health Reporter For Mailonline
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A genetic variant which may protect against Alzheimer's has been uncovered by researchers in a potential breakthrough.

Scientists at Washington University in St Louis analysed spinal fluid samples from around 800 participants. Some had the memory-robbing disorder.

Variations - Gene - MS4A4A - Levels - Protein

They discovered variations in the gene MS4A4A altered levels of a protein heavily linked to Alzheimer's, called TREM2.

Some variants were linked with either higher levels of the protein, which scientists said appeared to reduce the risk of Alzheimer's.

Others - Levels - TREM2 - Results - Risk

Others were linked to lower levels of TREM2, which the results suggested increased the risk of the disorder.

TREM2 is thought to 'ingest' the proteins amyloid β and tau, which cause the tell-tale plaques in an Alzheimer's patient's brain.

Researchers - MS4A4A - 'target - Alzheimer - Treatments

The researchers now hope MS4A4A could be a 'target' for future Alzheimer's treatments. It is currently incurable, with existing therapies only being able to temporarily ease symptoms.

Dementia affects 850,000 people in the UK, of which 62 per cent have Alzheimer's – the most common form, according to the Alzheimer's Society.

US - People - Condition - Alzheimer - Association

And in the US, 5.8 million people live with the condition, which is set to rise to nearly 14 million by 2050, Alzheimer's Association statistics show.

TREM2 is known to play a 'critical role' in the activation and survival of microglial cells, the researchers wrote in the journal Science Translational Medicine.

Form - Immune - Cell - Neurones - Health

These are a specialised form of immune cell that removes damaged neurones and maintains the health of the central nervous system.

A past study suggested variations to TREM2 increase the risk of Alzheimer's by almost three times. However, TREM2's exact role in the disease is 'not well understood'.

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