Alzheimer’s disease is commonly associated with memory loss, which is one of its most noticeable symptoms. However, there’s still much to learn about the biological processes that lead to these symptoms. Scientists are gradually putting all the pieces together.
A new mechanism. A team of researchers from Spain’s Severo Ochoa Center for Molecular Biology has discovered a new mechanism linked to the early development of Alzheimer’s disease. The key component of this mechanism is a protein called SFRP1.
The team has published its findings in Cell Reports.
Astrocytes and the SFRP1 protein. Astrocytes, a type of glial cell in the brain, play a crucial role in this newly identified mechanism. For some time, astrocytes were thought to be merely supportive cells for neurons, but their significance is becoming increasingly apparent.
In a mouse model, the study demonstrated that astrocytes may contribute to the onset of Alzheimer’s disease through the “excessive” production of the SFRP1 protein. This protein is involved in regulating communication between several cells during development. However, its overproduction later in life may pose significant risks.
A “traffic jam” in the brain. According to researchers, the accumulation of the SFRP1 protein in the adult brain is linked to chronic inflammation, often associated with aging and Alzheimer’s disease. The issue arises because this excess of SFRP1 protein blocks the activity of the enzyme ADAM10, which is essential for maintaining proper neuronal connections.
“This blockage creates an imbalance that disrupts synaptic plasticity, a crucial cellular mechanism for forming and consolidating memories. It allows neurons to adjust their connectivity in response to several stimuli,” researchers said in a press release.
Long-term potentiation. The accumulation of the SFRP1 protein interferes with a process known as long-term synaptic potentiation (LTP). This process is fundamental for learning and memory because it plays a vital role in brain plasticity. LTP reinforces the neuronal connections we use most frequently, which is essential for consolidating new memories.
A possible trigger. The battle against Alzheimer’s is essentially a race against time. The earliest noticeable effects of the disease are linked to irreversible damage in the brain, which often leaves doctors with the only viable option of delaying the progression of the disease.
Recent techniques aimed at detecting internal signs of Alzheimer’s, particularly the accumulation of amyloid plaques in the brain, may allow doctors to identify the disease before external symptoms appear. The recent study has opened a pathway to detecting even earlier stages of the disease.
“The increase of SFRP1 in early stages seems to act as an active driver of the pathology, rather than just a mere facilitator of other degenerative processes,” co-author Guadalupe Pereyra explained.
Beyond mouse models. Like any research conducted on mice, drawing broad conclusions from these findings can be challenging. Further studies are needed to validate these results and determine their relevance to the development of the disease in humans.
Translating these discoveries into new therapeutic approaches will also be a complex task. However, this type of progress is invaluable for several reasons. First, understanding the disease and its underlying mechanisms is crucial for discovering a future cure. Second, early detection provides a significant advantage in combating the disease’s symptoms.
Image | Steven HWG
Related | Researchers Develop a New Way to Diagnose Alzheimer’s Disease: A Simple Head Turn
View 0 comments