A recent study published in Science may change the way scientists see Alzheimer’s disease development : tau phosphorylation induced by the amyloid-beta plaque-forming protein is not promoting Alzheimer’s disease. It seems to have a protective effect.
According to the Australian researchers behind the study, phosphorylation of tau would in fact initially have a protective effect on neurons. Amyloid-beta accumulation would then challenge this protective layer until it is lost. When that step is reached, toxicity levels of tau cause neuronal death and eventually lead to cognitive deficits.
The researchers made that discovery after they noticed the low amounts of a protein named kinase p38γ in the brains of people with Alzheimer.
When reintroducing that protein in the brain of an Alzheimer mouse model, they noticed it could lower their memory deficits, has if the protein had a protective effect.
Researchers behind the study explain that stimulating p38 activity may help delay or even halt the progression of Alzheimer’s disease, providing a new pharmacological way to explore.