Across conditions as different as spinal cord injury, stroke, multiple sclerosis, and Alzheimer’s disease, a common thread keeps emerging: much of the long-term damage is driven not just by the initial insult, but by the body’s own biological response to it. Iron overload and ferroptosis, runaway ATP signaling, chronic inflammation, and immune imbalance can all turn a localized injury into widespread neural dysfunction.

A new wave of research is beginning to rethink how we intervene. Instead of targeting a single molecule or pathway, scientists are engineering multi-pronged strategies—nanoparticles that simultaneously block cell death and calm inflammation, precision immune therapies that redirect T cells toward pathological proteins, and receptor-based approaches that rebalance harmful signaling cascades after stroke or autoimmune attack. Together, these studies point toward a more integrated model of neuroprotection—one that treats inflammation, metabolism, and immune signaling not as side effects of disease, but as central levers for recovery.

1. Adipose-Specific GHR Deletion Attenuates Brain Aging and Cognitive Decline in Aged Mice

Deleting the growth hormone receptor specifically in adipose tissue reduced neuronal loss, neuroinflammation, cellular senescence, and tau phosphorylation in aged mice. Synaptic integrity and neuronal excitability were preserved, leading to significant improvements in memory and learning. The findings position adipose GH signaling as a powerful peripheral regulator of brain aging and a promising target to combat age-related cognitive decline.

2. Purinergic signaling in Stroke and Multiple Sclerosis: Prospects for therapies

Spatial transcriptomics in the PS19 mouse reveals that glycolysis pathway genes—particularly Pgk1—are upregulated in the hippocampal CA3 region before overt tau tangle formation. These early metabolic shifts, alongside emerging glial activation, suggest that energy dysregulation is an upstream event in tau-driven neurodegeneration, highlighting metabolism as a potential early intervention target in Alzheimer’s disease and related tauopathies.

3. Engineering chimeric antigen receptor CD4 T cells for Alzheimer’s disease

In a rat model of Cerebral ischemia–reperfusion injury, acupuncture reduced infarct volume, improved neurological scores, and preserved mitochondrial integrity. Mechanistically, it suppressed neuronal ferroptosis by restoring iron homeostasis through the IRP2/IRE pathway, lowering Fe²⁺ overload and oxidative stress while enhancing GPX4 and GSH activity

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