Secondary thalamic neuroinflammation after focal cortical stroke and traumatic injury mirrors corticothalamic functional connectivity
Abstract
While cortical injuries, such as traumatic brain injury (TBI) and neocortical stroke, acutely disrupt the neocortex, most of their consequent disabilities reflect secondary injuries that develop over time. Thalamic neuroinflammation has been proposed to be a biomarker of cortical injury and of the long‐term cognitive and neurological deficits that follow. However, the extent to which thalamic neuroinflammation depends on the type of cortical injury or its location remains unknown. Using two mouse models of focal neocortical injury that do not directly damage subcortical structures—controlled cortical impact and photothrombotic ischemic stroke—we found that chronic neuroinflammation in the thalamic region mirrors the functional connections with the injured cortex, and that sensory corticothalamic regions may be more likely to sustain long‐term damage than nonsensory circuits. Currently, heterogeneous clinical outcomes complicate treatment. Understanding how thalamic inflammation depends on the injury site can aid in predicting features of subsequent deficits and lead to more effective, customized therapies.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Nov 01, 2021
- Source ID
- 10.1002/cne.25259
Entities
People
- Andrea He
- Deanna Necula
- Frances S Cho
- Jeanne T. Paz
Organizations
- Gladstone Institutes
- National Institute of Neurological Disorders and Stroke
- United States Department of Defense
- University of California, San Francisco