Summary: Scientists have discovered a way to induce a hibernation-like state that protects the brain after injury—without using external cooling. By activating a specific population of neurons, researchers created a reversible drop in body temperature that preserved neuron health and improved motor recovery in mice.
Brain imaging revealed reduced inflammation and greater neuron survival in damaged regions. This breakthrough could one day offer a safer, controlled method to harness hypothermia’s neuroprotective effects in treating traumatic brain injury.
Key Facts:
- Internal Hypothermia: Activating certain neurons triggered a reversible, hibernation-like state that lowered body temperature.
- Neuroprotection: Mice treated this way showed better motor performance and neuron survival after brain injury.
- Reduced Inflammation: Brain imaging revealed less neuroinflammation in injured tissue compared to controls.
Source: SfN
Hypothermia can preserve neuron health following brain injury, but complications from external cooling make it less promising therapeutically.
Recent evidence suggests that activating a specific neuron population triggers a reversible, hibernation-like hypothermic state without external cooling, but does this form of hypothermia still preserve neuron health?
In a new Journal of Neuroscience paper, researchers led by Takeshi Sakurai at the University of Tsukuba explored this question using male mice.
The researchers found that triggering this specific hypothermic state in mice improved motor performance following brain injury. Imaging methods showed that neurons also had improved survival in the injured brain area accompanied by less signs of neuroinflammation.
The researchers further identified cellular features consistent with the idea that this form of hypothermia may preserve neural health.
While this work is preclinical, the authors suggest that it unveils a potential way to work around complications from external cooling when using hypothermia as a treatment for traumatic brain injury.
Speaking on future experimental plans, says Sakurai, “Optimizing the timing and duration of this treatment after injury, testing across additional injury models, and evaluating safety and efficacy in larger animals will be important next steps.”
Key Questions Answered:
A: Hypothermia therapy lowers body temperature to slow cellular damage and inflammation after injury, preserving neuron health.
A: Instead of using external cooling, researchers triggered a natural, neuron-driven hypothermic state similar to hibernation.
A: It could help develop safer, more precise hypothermia-based therapies without complications linked to external cooling.
About this neurology research news
Author: SfN Media
Source: SfN
Contact: SfN Media – SfN
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Q Neuron-Induced Hypothermia Promotes Functional Recovery and Suppresses Neuroinflammation After Brain Injury” by Takeshi Sakurai et al. Journal of Neuroscience
Abstract
Q Neuron-Induced Hypothermia Promotes Functional Recovery and Suppresses Neuroinflammation After Brain Injury
Traumatic brain injury (TBI) triggers a cascade of secondary pathologies—such as neuroinflammation and glial activation—that contribute to progressive neuronal loss and hinder functional recovery.
While therapeutic hypothermia has shown neuroprotective potential, its clinical application is limited by systemic complications.
Recent discoveries have identified hypothalamic Q neurons, whose activation induces a reversible, hibernation-like hypothermic state, termed Q neurons-induced hypothermic/hypometabolic states (QIH), without the need for external cooling.
However, whether QIH can mitigate brain injury remains unknown.
In this study, we examined the therapeutic effects of QIH following acute brain injury in male mice. Using a dorsal striatal stab injury model, we found that QIH-treated mice displayed significantly improved motor performance and grip strength compared to controls.
Histological analyses revealed enhanced neuronal survival in the perilesional striatum, accompanied by markedly reduced astrocytic gliosis and microglial accumulation at the injury site.
To investigate the mechanisms underlying these improvements, we employed a medial prefrontal cortex injury model and observed that QIH robustly suppressed astrocytic and microglial activation, as indicated by reduced GFAP and Iba1 expression.
Additionally, QIH decreased the number of CD16/32- and CD68-positive microglia and downregulated iNOS expression, suggesting that QIH dampens both oxidative and phagocytic inflammatory responses.
Morphometric analysis further revealed a shift toward ramified and rod-shaped microglia; phenotypes associated with neuroprotection. Our findings demonstrate that QIH ameliorates early neuroinflammation, preserves neuronal integrity, and promotes functional recovery following brain injury.
These results highlight QIH as a novel and physiologically grounded neuroprotective strategy that may overcome the limitations of conventional hypothermia-based interventions.
