Happy news about animals
A study conducted by University of Leeds researchers suggests that proteins that cause mad cow disease may be exploited to protect against Alzheimer’s.
In laboratory tests, the researchers observed that high levels of the prions in the brain prevented the accumulation of beta amyloid, the building blocks of Alzheimer’s ‘plaques’.
Study leader Professor Nigel Hooper says that the findings, published in the Proceedings of the National Academy of Sciences, are significant as they may lead to the development of new treatments for the disease.
In the human version of mad cow disease called variant Creutzfeldt-Jakob disease (vCJD), the infectious prions corrupt the normal version of the prion protein present in brain cells, causing them to change their shape which in turn results in brain damage and death.
Given that Alzheimer’s and variant CJD are similar, the researchers looked for a link between the two diseases.
They found that the build-up of beta-amyloid protein was reduced when the levels of prions were high in the brain. Whereas, the formation of plaques went back up again when the level of the prions was low or absent.
The findings, which have also been confirmed by experiments on mice genetically engineered to lack the prion proteins, suggest that the prions may have a preventive effect on the development of Alzheimer’s.
The researchers are now planning to study whether ageing has an effect on the ability of the prion proteins to protect against Alzheimer’s.
‘Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer’s plaques,’ the BBC quoted Professor Hooper as saying.
‘Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don’t know yet,’ he added.
He further said that more research was needed to determine whether the effects of the prions could be imitated to develop a treatment to halt the progression of Alzheimer’s.
The Alzheimer’s Society has hailed Professor Hooper’s findings by saying that this is the first time a link has been established between prions and Alzheimer’s.
‘These are early findings, which suggest prion proteins may have a regulatory effect on the development of beta amyloid,’ said Professor Clive Ballard, Director of Research, Alzheimer’s Society.
‘This provides the foundations for a novel approach to finding new therapeutic targets in Alzheimer’s disease,’ he added.