“Self-eating” refers to a normal process called cell autophagy, through which the body destroys bacteria and viruses after infection.
The process also counteracts neurodegenerative conditions such as dementia and Huntington’s Disease by getting rid of unwanted proteins and their resultant harm to cells. By contrast, when autophagy fails or defects occur, it can give rise to such conditions.
The mechanisms behind autophagy and how it progresses have been studied, particularly about the process called liquid-liquid phase separation (LLPS), which can provide the first steps towards new treatments for neurodegenerative diseases.
How the cell “eat” itself
The process of autophagy clearing cell wastes involves two steps:
Step 1, a protein called p62 binds a number of identical molecules together (called oligomerization);
Step 2, p62 separates the molecules within cell fluid, which is known as liquid-liquid phase separation (LLPS).
As for how p62 LLPS is regulated in cells, scientists have discovered that the process is facilitated by another protein called DAXX.
Dr. Luo, who focuses on finding new autophagy pathways and novel treatments for dementia diseases, said, "By understanding more about autophagy and the details of the processes involved, we can identify what might be going wrong, and therefore where to target when it comes to tackling neurodegenerative diseases. This research is a major step in helping us to do that.
"The next step for us is to look at applying the science within human cells, so we can further clarify how the protein interaction and the new DAXX function are relevant to neurodegenerative conditions including HD, and whether we can target it to help prevent disease progression.
"HD is an inherited disease that causes the progressive breakdown of nerve cells in the brain. It has a broad impact on a person's functional abilities and currently there is no cure, so it's vital that we continue our work to find out how and why the disease develops."