Neurological conditions such as amyotrophic lateral sclerosis, stroke, and spinal cord injury can worsen when the nervous system’s cleanup, immune, and energy-regulating processes begin to fail. These studies explore different ways to restore those functions. In ALS models, blocking SGK1 improved microglia’s ability to clear damaged myelin and neuronal debris, leading to better motor function and longer survival. In cerebral ischemia and reperfusion injury, Hspb1 reduced oxidative stress, inflammatory activity, and iron-related cell death in microglia, helping protect brain tissue.
The third study uses a therapeutic engineering approach, with a zinc-coordinated nanoassembly designed to respond to the harmful environment created after spinal cord injury. The treatment reduced inflammation and oxidative stress, supported mitochondrial recovery, protected neurons, and improved movement in mice. Together, these findings show how targeting immune cell function, cellular stress, and energy balance may help limit secondary damage in several serious neurological conditions while opening new directions for treatments that support recovery and repair.
1. SGK1-mediated deficits in microglial phagocytosis drive pathological progression in amyotrophic lateral sclerosis
SGK1 may impair microglia’s ability to clear myelin and neuronal debris in ALS models. Blocking SGK1 improved debris clearance, motor function, and survival in SOD1-linked ALS mice.
2. Hspb1 inhibits microglial ferroptosis and pro-inflammatory activation to alleviate cerebral ischemia/reperfusion injury in mice
Hspb1 helped protect the brain after ischemia/reperfusion injury by reducing microglial ferroptosis, oxidative stress, and pro-inflammatory activation. Its effects appear tied to regulation of the NF-κB/GPX4 pathway.
3. A zinc-coordinated cascade-responsive therapeutic nanoassembly for remodeling the pathological microenvironment and restoring mitochondrial homeostasis in spinal cord injury
A zinc-coordinated nanoassembly helped reduce inflammation and oxidative stress after spinal cord injury while supporting mitochondrial recovery. In mice, it protected neurons, improved tissue repair, and supported better motor function.
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