UK Researchers Halt Brain Cell Death in Mice

UK researchers have exposed the basis of what could become a new method to treat degenerative brain illnesses such as Alzheimer’s and Parkinson’s.

Scientists from the University of Leicester have, by tackling a new pathway, managed to stop brain cell death in mice with prion disease, a progressive disorder that affects the nervous system in humans (Creutzfeld-Jakob disease) and animals and damages brain function.

Several neuro-degenerative diseases result in the build-up of proteins which are not put together correctly – known as misfolded proteins. This happens in Alzheimer’s, Parkinson’s and Huntington’s, as well as in prion diseases, such as the human form of mad cow disease.

The research, which was published in the journal Nature and funded by the Medical Research Council, showed that the accumulation of such mis-shapen proteins triggered cells to stop creating new proteins altogether, which resulted  in synaptic death and neuronal loss in the brains of the mice which were studied.

This is the same trick that cells use when infected with a virus. Preventing the production of proteins stops the virus spreading. However, shutting down the production of proteins for a long period of time results in killing the brain cell as it does not create the proteins the cells need to work.

And critically, the study found that averting this transient shut-down of protein production helped protect the brain from cellular death, a finding that could possibly have major repercussions in the treatment of brain diseases, as it has exposed a common target underlying different clinical conditions.

Despite being in the very early stages, the data has generated a lot of excitement, as it has provided researchers with a new base to develop a therapy that could treat all diseases where protein misfolding leads to brain cell death.

Common mechanism

“What’s exciting is the emergence of a common mechanism of brain cell death, across a range of different neurodegenerative disorders, activated by the different mis-folded proteins in each disease,” noted lead researcher, Giovanna Mallucci.

“Instead of targeting individual mis-folded proteins in different neurodegenerative diseases, we may be able to target the shared pathways and rescue brain cell degeneration irrespective of the underlying disease,” she added.

Professor Andy Randall, from the University of Bristol, stated that “it will be interesting to see if similar processes occur in some of the common diseases with such deposits, for example Alzheimer’s and Parkinson’s disease.”

“Furthermore, if this is the case, can modulating this same pathway be a route to new therapeutic approaches in these more prevalent conditions that afflict many millions of sufferers around the world? Ultimately only more research will tell us this,” he added.

The research study has been largely welcomed by other scientists although several point out that the research is in its infancy.

Alzheimer’s disease and related disorders currently affect more than seven million people across Europe, but this number is anticipated to double every 20 years with the ageing population, highlighting the enormous challenge facing healthcare systems worldwide.


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