By comparing these two cases, the researchers found significant similarities and differences. Amyloid plaques, which many researchers believe play a significant role in Alzheimer’s disease, were abundant in the brains of both patients. However, the woman studied had low levels of another possible cause of Alzheimer’s: clumps of proteins called tau tangles. According to researchers, this is what kept the woman safe from dementia for decades; Because tau, more than amyloid, is thought to be associated with Alzheimer’s symptoms.

Researchers have obtained a different picture of tau in the brain of a Colombian man. “Unlike the Christchurch case, the man with the mutation was strongly affected by tau,” says Sepulvada-Fala. This issue surprised us at first; But in the end, we came to the conclusion that we need to do more in-depth investigations.”

In their investigations, the research team found that some areas of the brain, especially the entorhinal cortex, were spared from the accumulation of tau. The entorhinal cortex is very important in memory and is one of the first areas affected by Alzheimer’s disease.

The difference in tau between two cases with mutations is related to the difference in the activity location of the protective gene in the brain. In the adult brain, the reelin gene is active in only a few regions, including the entorhinal cortex, while the APOE gene is active everywhere. By the way Sepulvada FalaDue to the widespread presence of APOE in different parts of the body, the patient gets comprehensive protection. In the other case, the protection is focused on specific neurons, which happen to be the neurons involved in maintaining the cognitive process.

Although the genes work differently, they both produce proteins that bind to the same molecules on cells and ultimately appear to reduce the formation of tangled tau. Sepulvada Falla and colleagues confirmed this using mice genetically engineered to produce tau.

Introducing Reelin-Colbus mutants into mice prevented the accumulation of tangled tau. According to the researchers, this mechanism, which is common to both mutations, can be targeted by new treatments with the aim of preventing the occurrence of Alzheimer’s types.

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