From multiple sclerosis to spinal cord injury and vascular dementia, many neurological diseases share a common thread: chronic inflammation, oxidative stress, and difficult-to-target cellular damage. But recent studies are revealing innovative ways to interrupt these destructive processes—offering new hope for conditions long considered resistant to treatment.
One team has uncovered a key molecular pathway driving neuronal ferroptosis in vascular dementia, providing a clearer map for how nerve cells succumb to oxidative stress. Another group is harnessing stem cell–derived exosomes to deliver a potent ferroptosis-blocking enzyme right where it’s needed in spinal cord injury. Meanwhile, researchers exploring CAR-T cell therapy in progressive MS show that targeting plasma cells in the brain could calm inflammation and potentially slow disease progression. Together, these findings highlight a growing shift toward precision strategies that modulate immune and oxidative pathways—helping the nervous system better protect and repair itself.

1. The KLKB1-TFE3-BRAF/MEK/ERK axis regulates neuronal ferroptosis in vascular dementia
Bioactive compounds from brown, red, and green seaweeds show potential in targeting multiple pathways involved in Alzheimer’s disease, including oxidative stress, neuroinflammation, amyloid accumulation, and synaptic dysfunction. This review highlights emerging evidence that these marine-derived nutrients may support cognitive resilience and offer a safer, multi-targeted approach to slowing age-related neurodegeneration
2. Targeted delivery of the GPX4 activator via HUCMSC-derived exosomes inhibits ferroptosis in spinal cord injury
Oral dihydroquercetin improved motor and sensory function in SCI rats by reducing ferroptosis, oxidative stress, and neuroinflammation. These effects were mediated through activation of the AKT/Nrf2/GPX4 signaling pathway, highlighting a promising neuroprotective mechanism for post-injury recovery.
3. Anti-BCMA CAR-T therapy in patients with progressive multiple sclerosis
Anti-BCMA CAR-T therapy in progressive MS patients led to deep plasma cell depletion in the CNS, sustained CAR-T cell presence in cerebrospinal fluid, and reduced neuroinflammation—pointing to a promising strategy for modifying hard-to-treat disease progression.
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