Removing Tau Protein Build-Up in Your Brain Cells
Haung (Ho) Yu, PhD, Columbia
- Why does tau build up in your neurons in aging diseases?
- Tau was originally described as helping to facilitate function, but sometimes it gets disrupted in your brain cells and disrupts multiple types
- We want to see if we can reverse this
- With aging and disease, the regulation of these systems decline, we are trying to figure out why, and how we can boost them
- What is autophagy? (Cell’s way of self-eating) and why is it an important in removing “garbaging” cells?
- Proteasome – removes unfolded soluble proteins
- Break down the cells so that they can be rebuilt
- Identifying where this takes place is very important,
- Autophagy – remove aggregates following autophagic induction
- Lysosome – degrade most proteins – lysosomal acidification
- Proteasome – removes unfolded soluble proteins
- Autophagy – the good and the bad
- In early stage diseases, the “garbage” collecting isn’t happening fast enough
- Later on in disease, these processes become even more destructive, so we want to improve the pathways or the entry to recycling center
- If the “recycling center” itself is disrupted (in most neurodegenerative diseases), that can cause problems too
- Can you see clearance of garbage in imaging and where it builds up, and are there patterns?
- Yes, some transport is probably being taken place but not efficiently
- Want to improve the entire process, most treatments work on early on disease, but with these diseases the onset happens quickly.
- Goal is the bring the deliverers and recycling centers together
- Does dependent reduction in aggregated and soluble tau levels matter?
- Trying to identify potential drugs that can enter the brain and start to treat the diseases
- Challenge is, can we improve the drug to enter the brain and last longer?