2024-01-17 12:39:22
Subtype1 (neuronal hyperplasticity)
At 32 percent, it affected most of the patients examined. The researchers saw the highest concentration of proteins from different brain cell types in this group of patients. They describe the underlying disease mechanism as “neuronal hyperplasticity”:
The term refers here to one increased activation of nerve cells (neurons) in the brain. This apparently contradicts the understanding of Alzheimer’s, which is associated with a loss of neurons.
However, neurons with increased activity produce more of the proteins that form the typical Arzheimer deposits (amyloid beta and tau proteins). These deposits cause, accelerate or accompany the death of nerve cells. We don’t know exactly yet. In any case, “hyperactive neurons […] observed near plaques,” the researchers write.
They also suspect one Disruption of the function of certain immune cells (Microglia) as a disease driver in Alzheimer’s subtype 1. The task of microglia is to eliminate damaged cells and pathogens in the brain.
When activated, the immune cells also normally form a tight barrier around the Alzheimer’s plaques. In this way they form a protective barrier for nerve cells.
People with Alzheimer’s subtype 1 often carry a specific gene variant (TREM2) that dampens the activity of microglia. “Then the amyloid plaques are less compact,” write the researchers. The result: Destructive molecular complexes (toxic oligomers) protrude from the microglial barrier and damage the neighboring nerve cells.
It may be possible to counteract this in the future: drugs that affect the activity of TREM2 are currently being tested.
#faces #Alzheimers