Sticky proteins associated with degenerative brain diseases can be transferred

‘Transmissible’ Alzheimer’s theory gains traction

Mouse tests confirm that sticky proteins associated with degenerative brain diseases such as Alzheimer’s can be transferred. However, researchers say risks for humans are likely to be minimal. The study published in Nature showed that it is possible for the amyloid protein to transfer under particular conditions, and to cause damage in a recipient’s brain.

Contagious
The researchers stress that their findings do not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

Amyloid-beta deposits
The work follows up on a provocative study published by researchers from University College London in 2015. The scientists discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

Amyloid plaques
The recipients had died in middle-age of Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. The researchers suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Cerebral amyloid angiopathy
Amyloid plaques in blood vessels in the brain are a hallmark cerebral amyloid angiopathy (CAA). In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

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