In Brief
  • A new study in mice signals how manipulating the tau protein via the enzyme p38γ kinase could prevent Alzheimer's disease.
  • The technique is novel because most of the research on Alzheimer's centers around beta-amyloid levels in the brain that's suspected of causing plaques associated with the disease.

PREVENTING PROTEIN PROBLEMS

Alzheimer’s disease is a debilitating condition where toxic changes in the brain cause disruptions in memory and cognitive reasoning. Although there are several ongoing studies and clinical trials on the condition, an Alzheimer’s cure remains unavailable.

But a study from scientists at the University of New South Wales, Australia could unlock the mystery of a cure. The study suggests the condition can be prevented by stopping the malfunction of a single protein in the brain, according to research on mice published in Science.

The protein, called tau protein, normally functions as a stabilizer for the microtubules that act as rails for transporting materials around the cell. As New Scientist reported, studies have suggested problems with the tau protein is somehow linked to Alzheimer’s. The protein can clump together in twisted tangles and could be releasing Alzheimer’s-inducing toxic chemicals.

Neurofibrillary tangles of tau protein in the hippocampus of an old person with Alzheimer’s-related pathology. WikiMedia.
Neurofibrillary tangles of tau protein in the hippocampus of an old person with Alzheimer’s-related pathology. Image Credit: WikiMedia.

In studies on mice, an enzyme called p38γ kinase interfered with the accumulation of the protein called beta-amyloid — another suspected cause of Alzheimer’s. The tangling of beta-amyloid appeared to cause a domino effect that sets off the clumping of tau proteins.

Lars Ittner, together with his colleagues, discovered how hindering the beta-amyloid mutation using p38γ kinase also stopped tau protein from tangling. Mice that were bred to develop Alzheimer’s didn’t develop the disease when the enzyme was present in high levels.

TOWARDS A CURE

Previously, enzyme therapies were directed toward reducing beta-amyloid mutation but found little success. This development shows greater potential with its effectiveness in animal studies. Ittner also said their study could transition to human use more easily because the models were designed to recreate the relationship of the proteins beta-amyloid and tau in humans.

“I think this is very, very exciting. Our focus has been on beta-amyloid but this gives the tau approach a really good kick,” Ittner said, according to New Scientist.

It could be several more years of research before the study fully transitions into an effective treatment for humans, but more and more scientists are taking steps toward a cure. Studies like this are on track to improve the lives of the estimated 4.4 million people worldwide suffering from Alzheimer’s disease.