Mechanism that contributes to the early development of Alzheimer's discovered

Researchers from the Severo Ochoa Center for Molecular Biology, in collaboration with the Pablo de Olavide University of Seville in southern Spain and VU University Amsterdam , have identified a new mechanism that contributes to the early development of Alzheimer's disease, long before the appearance of its classic signs.

The study, which was reported on May 8 by the Spanish National Research Council (CSIC) in a statement, focuses on the so-called 'astrocytes' , brain cells that were long considered mere helpers to neurons.

Researchers have shown in a mouse model that these astrocytes may, however, play a "key role" in the origin of Alzheimer's, through the excessive production of a protein called 'SFRP1'.

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Under normal conditions, this protein regulates communication between cells during brain development. However, its accumulation in the adult brain, as occurs during chronic inflammatory processes associated with aging or Alzheimer's disease, has detrimental effects.

In excess, SFRP1 blocks the activity of an enzyme —that is, a protein that facilitates and accelerates functions in the brain—, called 'ADAM10', which is necessary to maintain healthy neural connections. This blockage creates an imbalance that impairs an essential cellular mechanism for forming and consolidating memories, allowing neurons to regulate their connectivity in response to different stimuli.

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The study also shows how excess SFRP1 interferes with a fundamental process for learning and memory, which allows connections between neurons to strengthen when used repeatedly, facilitating the consolidation of new memories.

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

The findings position SFRP1 as an emerging therapeutic target in the fight against Alzheimer's, with the potential to intervene in the early stages of the disease, before irreversible neuronal damage occurs.

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