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The cause of Alzheimer's disease is linked to a mutation in an enzyme

Researchers from Tokyo Metropolitan University have discovered a new mechanism by which clots of Tau protein are created in the brain that kill brain cells and cause Alzheimer's disease. 

Author: Bolysbek Dana 

Translator: Tursunova Balkadisha 

Editor: Aigerim Akhmetova    



Alzheimer's Is a debilitating, life –changing condition that affects tens of millions of people around the world. According to the world health organization, it is the most common cause of senile dementia, and its number worldwide is expected to double every 20 years if left unchecked. 


Alzheimer's is thought to be caused by the accumulation of clumps of Tau protein in brain cells. These glomeruli cause the death of neurons that leads to impairment of memory and motor functions. It is not yet clear how or why Tau protein accumulates in the brain cells of Alzheimer's patients. 


A team of scientists led by associate Professor Kane Ando from Tokyo Metropolitan University studied the role played by the enzyme MARK4 (kinase 4, which regulates affinity for microtubules) in Alzheimer's disease. Normally, Tau protein is a protein that is involved in the formation of microtubules (cytoskeletal structures). The MARK4 enzyme helps the Tau protein detach from microtubules in time. 


The researchers artificially made point changes to the genome of transgenic fruit flies, which also produce human Tau protein, and studied how the proteins change in vivo. As a result, they found that this mutant form of the MARK4 enzyme makes changes to the Tau protein, creating a pathological form. This Tau protein contained an excess of certain chemical groups, making it more prone to aggregation and more insoluble. This made it easier for the Tau protein to form tangled clusters that cause neuron degeneration. 


MARK4 has also been found to cause a wide range of other diseases related to aggregation and accumulation of other proteins. Thus, the team's findings about Tau protein accumulation may lead to new treatments and preventive measures for an even wider range of neurodegenerative conditions.