We generally associate Alzheimer’s disease with memory loss since this is probably its most visible symptom. However, it is still what we do not know about the biological processes that unleash these symptoms. Piece by piece, we are solving this immense puzzle.
New mechanism. A team in which researchers from the Severo Ochoa Molecular Biology Center (CBM-CSIC-UAM) have discovered a mechanism linked to the early development of Alzheimer’s disease. The key component of this mechanism is in a protein called SFRP1.
Astrocytes and SFRP1. As described by the team responsible for the finding, in the origin of the mechanism are brain cells called astrocytes. Astrocytes are glial cells (a type of nerve cell) that for a while we thought they exercised as “assistants” of neurons but whose relevance we are seeing grow.
In a mice -based model, the new study has shown that these cells could play an important role in the appearance of Alzheimer’s through an “excessive” production of the SFRP1 protein. This protein is one of the compounds involved in the regulation of communication between different cells during development, but in later stages of life its excess may imply risks.
A “jam” in the brain. As the equipment continues, the accumulation of the SFRP1 protein in the adult brain is associated with chronic inflammatory processes associated with aging, and also to Alzheimer’s own disease. The problem arises when this excess blocks the activity of the adam10 enzyme, which plays a key role in maintaining the proper functioning of neuronal connections.
“This blockage generates an imbalance that deteriorates synaptic plasticity, an essential cell mechanism to form and consolidate memories that allows neurons to regulate their connectivity in response to different stimuli,” they explain in a press release.
Long -term synaptic potentiation. The accumulation of the SFRP1 protein would thus be interfering with a process called LTP or long -term synaptic potentiation. This is a “fundamental” process for learning and memory, the team stands out. A vital process in brain plasticity, that is, that allows the neuronal connections that are most frequently used to be reinforced, something indispensable when consolidating new memories.
The details of the study have been published in an article in the magazine Cell Reports.
A possible trigger. The fight against Alzheimer’s is a fight against the clock. The appearance of its most easily noticeable effects is associated with lesions already irreversible in the brain, so the only remaining route of action is to delay the advance of the disease.
The techniques focused on detecting the internal signs of the disease, mainly the accumulation of amyloid plaques in the brain can allow us to advance ourselves to the appearance of the external symptoms of the disease. Now, the new study opens a way to enter the still previous stages of the disease.
“The increase in SFRP1 in early stages seems to act as an active engine of the pathology, not as a simple companion of other degenerative processes,” Guadalupe Pereyra, co -author of the study, explains in the press release.
Beyond rodents. Like any study in mice, extrapolating its conclusions can be complicated, so studies that validate what you have learned and the degree to which it is applicable to the development of the disease in humans will be needed.
Converting what has learned into new therapeutic pathways will not be simple either, but this type of advance can help us in different ways. First, because understanding the disease and its mechanisms is essential in order to find a future cure; And second, since in the fight against its symptoms, early detection is a very important advantage.
In WorldOfSoftware | If the question is how to hunt the Alzheimer
Image | CSIC
