A mechanism has been discovered that can help detect Alzheimer's in its early stages.

A team of researchers from the Severo Ochoa Molecular Biology Center , together with Pablo de Olavide University and VU University Amsterdam (Netherlands), has discovered a mechanism that causes early changes in the brain long before the appearance of classic Alzheimer's symptoms , which may contribute to its early detection.

The study, published in the journal Cell Reports , shows that astrocytes in the brain may play a key role in the origin of this pathology, by overproducing the protein SFRP1, which regulates communication between cells during brain development.

Its excessive accumulation in the adult brain has harmful effects , as it blocks the activity of the ADAM10 protein, which facilitates and accelerates brain functions, in addition to being necessary to maintain healthy neuronal connections.

This blockage causes an imbalance that ultimately impairs synaptic plasticity , an "essential" mechanism for forming and consolidating memories; the study also shows that excess SFRP1 interferes with long-term synaptic potentiation, a process "fundamental" to learning and memory . The aforementioned structural alterations in neuronal synapses precede memory loss and the accumulation of amyloid plaques, previously considered one of the main markers of the disease; furthermore, they correlate "much more" with cognitive decline than the plaques themselves.

"The increase in SFRP1 in early stages appears to act as an active driver of the pathology, not as a simple companion to other degenerative processes," explained the study's author, Guadalupe Pereyra .

Similarly, it "deeply" affects the cycle of presynaptic vesicles , which are "essential" for communication between neurons , and increases the presence of proteins such as neurexin, involved in synaptic adhesion, a disruption that compromises neuronal plasticity and the consolidation of memories.

Acting during the silent but critical stage

All of these findings open the possibility of action being taken during this "silent but critical stage " of the disease, as it is a time when neurons can still recover.

Scientists have highlighted that the contribution of glial cells (such as astrocytes) to Alzheimer's is one of the "least studied," particularly in relation to the early changes observable in the brains of patients and in animal models, before the onset of neuronal degeneration.

During the research, a mouse model was developed in which SFRP1 overexpression was induced specifically in astrocytes, a manipulation that was "sufficient" to cause a progressive loss of synaptic spines in the hippocampus, as well as a rigidity in neuronal connections that limits their ability to adapt to new experiences.

For all these reasons, researchers have positioned the aforementioned protein as an "emerging" therapeutic target in the fight against this disease, with the potential to allow interventions in early stages and before irreversible damage occurs.