The researchers then wanted to test their hypothesis that the loss of BMI1 plays a direct role in the development of AD. To do so, they created healthy human neurons in the lab. Once the neurons reached maturity, they deactivated the BMI1 gene using a genetic method.
The results were truly spectacular. All the neuropathological markers of AD were reproduced in the lab. The researchers concluded that the loss of BMI1 function in human neurons was enough to trigger AD.
Encouraged by their unexpected findings, the researchers also ran molecular studies to understand how the loss of BMI1 triggers AD. These studies revealed that the loss of BMI1 causes an increase in production of beta-amyloid and tau proteins and a decrease in the neurons’ natural capacity to eliminate toxic proteins.