TYK2 was linked to inflammation in TDP-43-related brain disease
Original source
TYK2 mediates neuroinflammation in Alzheimer's disease brains with TDP-43 pathology. (opens in a new tab)Compass summarised this from the study's abstract.
Study details
- Studied in
- Human, Animal, Cells
Researchers linked the immune-signaling protein TYK2 to toxicity triggered by abnormal RNA and TDP-43 pathology in human brain tissue and laboratory models. Blocking TYK2 reduced this toxicity in the models studied, while two approved JAK inhibitors were protective only in models with higher signs of TDP-43 mislocalization.
Why this matters
The findings identify TYK2 as a possible target for TDP-43-associated disease, including C9ORF72-related ALS. However, the work was conducted in postmortem tissue and laboratory models, so it does not currently change treatment for people with ALS.
Limitations and context
The study did not test TYK2 inhibitors in people with ALS. Its evidence came from human postmortem tissue, induced pluripotent stem cell-derived neurons, and other laboratory experiments. Further clinical research is needed to determine whether TYK2 targeting is safe and beneficial in ALS.