HtrA1L364P Leads to Cognitive Dysfunction and Vascular Destruction Through TGF-β/Smad Signaling Pathway in CARASIL Model Mice
July 2022
in “
Brain and Behavior
”
Studysummary This study observed that a CARASIL mouse model demonstrated abnormal behavior, vascular and cellular changes, and upregulation of the TGF-β/Smad signaling pathway, indicating its potential involvement in CARASIL pathogenesis.
Our plain-language summary. Not medical advice or a treatment recommendation. Consult a qualified healthcare professional before changing treatment. Full disclaimer
The study on CARASIL model mice with the HtrA1L364P mutation demonstrated significant cognitive dysfunction and vascular damage through the TGF-β/Smad signaling pathway. Using 90 mice, researchers found that mutant mice had impaired learning and memory, disordered vascular structures, and increased TGF-β, Smad2, and Smad3 expression. Pathological analysis revealed endothelial cell hyperplasia and myelin sheath abnormalities. These findings suggest that the HtrA1L364P mutation disrupts TGF-β signaling, leading to ECM deposition and vascular pathology, which impairs brain function.
