Mitochondrial Double-Stranded RNA Drives Aging-Associated Cognitive Decline
Our brains, like the rest of our bodies, change as we age, often leading to a decline in memory and thinking abilities. While many factors contribute to this, recent research has uncovered a surprising culprit: tiny pieces of genetic material from within our cells’ powerhouses, the mitochondria.
These powerhouses, called mitochondria, contain their own genetic instructions, including something called double-stranded RNA. Normally, this RNA stays safely tucked away. However, a new study suggests that as we get older, a protein named SEC61A1, which helps manage the connections between mitochondria and another cell structure called the endoplasmic reticulum, can malfunction. The endoplasmic reticulum is like the cell’s factory and transportation system.
When SEC61A1 doesn’t work correctly, it allows these mitochondrial double-stranded RNA molecules to escape into the main part of the cell. Once outside, these rogue RNA molecules are seen as a threat by the cell’s internal defense system, known as the innate immune response. This defense system, specifically through a pathway involving a protein called MAVS, then kicks into overdrive, causing chronic inflammation in the brain.
This persistent inflammation is not good for brain cells and can lead to neurodegeneration, which is the progressive loss of brain cells, ultimately impairing memory and other cognitive functions. Researchers observed this pathway becoming active in aged mice and in brain samples from individuals with Alzheimer’s disease, suggesting it plays a significant role in both normal aging and neurodegenerative conditions.
This discovery opens up exciting possibilities for new treatments. By targeting SEC61A1 or the MAVS pathway, scientists hope to develop ways to prevent or even reverse the cognitive decline associated with aging and diseases like Alzheimer’s.
Source: link to paper