Sometimes realizing you’re wrong leads to great insight. That’s what happened when a team of Australian researchers from the University of New South Wales and Neuroscience Research Australia identified a protein, kinase p38y, that diminishes as Alzheimer’s disease progresses. Through their research, they have discovered that an important step in the development of Alzheimer’s disease has been misunderstood, and they have opened the doors to the possibility of slowing the progression of Alzheimer’s, or even stopping it altogether.
Lead author of the study, UNSW Professor Lars Ittner, says, “This study has completely changed our understanding of what happens in the brain during the development of Alzhemier’s disease.”
So what did they learn?
To understand this potentially groundbreaking discovery, you will need to understand a little about the mechanisms in the brain that are believed to cause Alzheimer’s. There are two hallmarks of Alzheimer’s development – the presence of toxic levels of protein plaques and tangles in the brain. The protein plaques are made up of amyloid-beta and the tangles are made up of tau protein. The accumulation of plaques and tangles are what researchers believe leads to cell death, brain atrophy (shrinking) and memory loss. Scientists used to believe that the amyloid-beta caused a modification of the tau protein. This modification is called phosphorylation (fos-for-a-lay-shun) and they believed that the phosphorylation of tau protein led to the accumulation of tangles.
But the UNSW team found evidence that the tau protein phosphorylation initially has a protective effect on brain neurons. It seems phosphorylation of tau occurs as the body’s defense against the plaque-forming amyloid-beta and associated toxicity. According to Professor Ittner, “Amyloid-beta induces toxicity in the neurons, but the first step in tau phosphorylation is actually to decrease this toxicity.”
Unfortunately, the body’s own defenses are not always strong enough. Researchers believe that Alzheimer’s develops as amyloid-beta continues to eat away at the protective function of the tau until it is lost. And at this stage, the amyloid-beta begins to induce toxic levels of plaques that damage the neurons and lead to the signs and symptoms of Alzheimer’s.
However, there is promising news. The kinase p38y protein we mentioned earlier has been shown to have a protective effect on brain neurons. The researchers isolated the kinase p38y and re-introduced it into the brains of mice. They found that kinase p38y assisted with protective phosphorylation of tau and also interfered with the brain tissue toxicity that the amyloid-beta created.
Kinase p38y is present in human brains, but as Alzheimer’s progresses, the protein and its protective effect are diminished. During the study, they found that re-introducing kinase p38y into the brains of mice had a protective effect against the memory deficits associated with Alzheimer’s.
The results of this study hold hope that at least one of the devastating effects of Alzheimer’s – memory loss – can be slowed or even stopped completely. Professor Ittner says that by re-introducing p38y they found that “in mice, it could prevent memory deficits from happening, so it has true therapeutic potential. If we can stimulate that activity [in the brain], we may be able to delay or even halt the progression of Alzheimer’s disease.”
Citation: University of Sydney. (2016, November 14). Brain training can help in fight against dementia, meta-analysis shows. ScienceDaily. Retrieved November 29, 2016 from www.sciencedaily.com/releases/2016/11/161114105531.htm