hope for treatment with brain-protecting protein

hope for treatment with brain-protecting protein
hope for treatment with brain-protecting protein

THE ESSENTIAL

  • Researchers have discovered that injecting a mutated protein could protect mice from Alzheimer’s disease.
  • After a single injection, they had an improvement in their memory for several months.
  • For the moment, these results have been observed in mice and will not necessarily be the same in humans.

900,000 people suffer from Alzheimer’s disease in France, according to the National Institute of Health and Medical Research (Inserm) and, for the moment, no curative treatment exists to cure them. But research is moving forward, as evidenced by this new study published in the journal Molecular Psychiatry.

A mutated protein injected into sick mice

To fully understand this new discovery, we must return to the origin of Alzheimer’s disease. This is due to two types of lesions: amyloid deposits and neurofibrillary degeneration.

Each of these lesions is associated with a protein: the amyloid beta peptide. (β-amyloid) for amyloid deposits, and phosphorylated tau protein for neurofibrillary tangles”, indicates Inserm. It is these lesions that alter the brain and therefore lead to memory loss.

In their work, the scientists used a mutated amyloid protein. This was already known to the scientific world – it was discovered in the Icelandic population – as having a protective effect against Alzheimer’s disease and cognitive decline.

They tested this mutated amyloid protein on mice suffering from Alzheimer’s disease, at the early stages of the pathology. The rodents were separated into two groups: one which, via a single injection into the brain, received this mutated protein, and the other, where nothing was administered.

The study lasted four months. Throughout this period, the researchers observed very good results: the mice in the first group were protected against Alzheimer’s disease!

In detail, in these mice, the accumulation of Tau protein was reduced, as was damage to neurons and synapses, the contact area between two neurons. The researchers also noted an improvement in their memory. On the other hand, there was no impact on amyloid deposits.

Towards a new treatment for Alzheimer’s disease?

These results are very encouraging but, for the moment, they have only been observed in mice and will not necessarily be the same in humans. “In the future, we will try to develop a gene therapy allowing this protein to be expressed more easily in the brain than through a local injection, the latter being less feasible in humans.”, indicates Marc Dhenain, research director at the National Center for Scientific Research (CNRS) and one of the authors of this study, in an interview with 20 minutes.

Clinical trials should therefore be carried out on humans to confirm these results, and perhaps, one day, use these mutated amyloid proteins to fight against Alzheimer’s disease and cognitive decline.

A hope because, by 2050, the number of people with dementia in Europe will almost double by 2050, rising to 14,298,671 in the European Union and to 18,846,286 in Europe as a whole, according to the forecasts ofAlzheimer Europe.

-

-

PREV Better monitoring for obesity
NEXT A Vendée woman is refused an “extension” of long-term sick leave to treat her breast cancer