Medical Network June 25, amyloid precursor protein (app) has been considered as the main cause of Alzheimer's disease. A fragment of it, an amyloid peptide, can divide and accumulate in the brain, causing a swollen white sphere called the senile plaque, a sign of the disease.
However, in a recent study published in the journal Cell Reports, researchers at the University of Chicago revealed the broad role of app in brain signaling.
a long-neglected part
Over the years, researchers have focused on the amino acid sequence encoded by the Aβ segment in APP, such as a dormant monster waiting to be released. However, in this new study, Associate Professor of Neurobiology Angele Parent and her team have shown that other parts of a shredded app chain are also important. One part plays a vital role in consolidating the temporal and spatial learning and memory of the brain, and it can prevent the onset of Alzheimer's disease when appropriate.
This long-neglected fragment, when attached to the cell membrane, can participate in a signaling mechanism that triggers the formation of new memories. To facilitate this connection, Parent and his team created a viscous lipid-anchored protein using a natural APP. This modified app fragment is called mAICD and is simple in structure but powerful. Six months after the mice were born, the researchers injected them with a virus that promoted high expression of mAICD in the brain, and the results were surprising.
These mice were genetically engineered to develop aggressive Alzheimer's disease at a young age. Under normal circumstances, if no additional mAICD researchers provided they advanced symptoms of the disease (the human equivalent of a young man) appearing at the six months time.
After the injection of the virus, Parent and her team tested the ability of mice to form space-time memory. A mouse is a curious but variable animal. With the help of mAICD, these mice successfully regained or ignored objects and places that were previously explored. On the other hand, control mice with Alzheimer's disease expressed less mAICD, and they did not recognize so-called familiar objects and locations at all.
"When we looked at mice that expressed mAICD, they almost became normal," Parent said. It is as if these mice have never shown signs of Alzheimer's disease.
This inconspicuous lipid-anchored protein inhibits Alzheimer's disease in these mice as long as its expression begins in the brain developmental stage. Researchers are currently investigating the effects of the same mAICD intervention on the brains of adult mice that already have Alzheimer's disease.
"If you have a gene for Alzheimer's disease, you don't necessarily have memory problems when you are young. All of this happens a long time later," Parent said. "At that time, when your memory is already problematic, can the rise in mAICD help you?"
In fact, the diversity of APP functions has exceeded the expectations of early researchers. By participating in complex neural mechanisms, APP triggers a series of events related to memory consolidation, stimulates the growth of new neurons, and enhances synaptic activity. At the same time, the app may also produce Aβ to weaken these memories.
This "universal protein" has many functions and occasionally contradicts each other. Despite this, Parent hopes that it will become a coveted memory molecule because of its ability to form and eliminate memory.
Reference materials:
Carole Deyts et al. APP-Mediated Signaling Prevents Memory Decline in Alzheimer's Disease Mouse Model, Cell Reports (2019). DOI: 10.1016/j.celrep.2019.03.087
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