How do Alzheimer's disease-causing plaques gather?

  The self-renewal ability of biological molecules (such as our DNA) is the foundation of life. Self-renewal is a process that usually involves complex cellular mechanisms. However, certain proteins can replicate without other help, for example, cause minor diseases The protein fibers (fibrils) are related to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. These fibers called "amyloid" entangled with each other, causing so-called "plaques" to be found in the brains of Alzheimer's patients.

  The first amyloid fibrils formed spontaneously are very slow, usually taking decades. This may explain why Alzheimer's disease is a disease that usually affects people later. However, when the first fibers are formed, they begin to self-replicate, spread themselves quickly, and ultimately make disease control very difficult. Despite its importance, it is not clear how to replicate the basic mechanism of protein fibers without using other mechanisms. In a study published today in the Journal of Natural Physics, a research team led by researchers from the Department of Chemistry at the University of Cambridge combined powerful computer simulations and laboratory experiments to require the self-renewal of protein fibrils. I confirmed it. status. The researchers found that the seemingly complex process of fiber self-renewal is actually controlled by a simple physical mechanism, that is, the accumulation of normal proteins on the surface of existing fibers. The researchers used a molecule called beta-amyloid, which constitutes the main component of amyloid plaques found in the brains of Alzheimer's patients. They found a link between the amount of normal protein deposited on existing fibers and the rate of fiber self-renewal. In other words, the larger the aggregated protein of amyloid fibers, the faster the self-renewal of plaques.

  They also found that, as a proof of principle, the self-renewal of fibers can be controlled by changing the way healthy proteins interact with the fiber surface. Andela Saric, the first author of the study, said: “One of the secrets of amyloid plaque formation is how fast amyloid plaque formation develops after a long and slow process. Fast. In fact, it makes the system catalyze it. Its own activity. It has been found that the process is out of control, but if it can control the establishment of normal proteins on the fibrils, the discovery limits the aggregation and spread of plaques. I believe this discovery may be very interesting in the field of nanotechnology. Realizing effective self-replication in the preparation of nanomaterials is one of the unfinished goals of nanotechnology. This is exactly what is observed between these fibers. Self-replication through this process. If we can learn design rules, we may be able to achieve this goal.