Biomimetic nanozymes reduce neuroinflammation and cognitive decline in aged mice
Neutrophil-coated nanoparticles crossed the blood-brain barrier, altered microglial metabolism, and improved cognitive performance after surgery in older mice.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Huang L et al. · Paper published 30 Sep 2026
In an aged mouse model of perioperative neurocognitive disorders, researchers tested a biomimetic nanozyme platform designed to target surgery-induced brain inflammation. The formulation, termed PCN, encapsulates palladium and hollow cerium oxide nanoparticles within neutrophil membranes. Leveraging the natural inflammation-homing properties of the cell membranes, the nanozymes crossed the compromised blood-brain barrier and accumulated in inflamed brain regions. The nanoparticles scavenged reactive oxygen species, lessened neuroinflammation, and preserved blood-brain barrier integrity. Within microglia, the treatment suppressed pro-inflammatory activity by inhibiting glycolysis and promoting aerobic respiration. These metabolic shifts protected synaptic function and improved cognitive performance in the aged mice.
Why it matters
Postoperative cognitive dysfunction is a major clinical issue in aging populations linked to heightened neuroinflammation and microglial activation. Interventions that reprogram brain immune metabolism and neutralize oxidative stress offer a targeted strategy to counter age-dependent inflammatory damage.
Caveats
The findings are restricted to aged mice undergoing an experimental model of surgery-induced cognitive disorder. Further research is required to evaluate whether the nanoparticle platform functions safely and effectively in humans.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
A Neutrophil Membrane-Encapsulated Pd/hCeO₂ Nanoformulation for Alleviating Age-Dependent Perioperative Neurocognitive Disorders
Huang L, Cheng J, Xu H et al.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 30 Sep 2026 · Peer-reviewed
- Relevance
- Relevant
- News value
- Notable
- Evidence
- Animals
- Status
- Peer-reviewed
More on Brain aging
See allHuman neurons accumulate far more mutations over lifespan than shorter-lived mammals
Cortical neurons gain mutations at similar yearly rates across six species, leaving aged humans with uniquely high mutational burdens and transcriptomic dysregulation.
bioRxiv : the preprint server for biology · Caglayan E et al.
CAR T cells targeting inflammatory bone marrow progenitors restore cognition in aged mice
Clearing these peripheral myeloid cells remodeled brain macrophages and improved cognitive performance without requiring the engineered immune cells to enter the brain.
bioRxiv · Harris AS et al.
Extracellular cGAMP drives neuroinflammation and premature aging phenotypes in mice
Loss of the cGAMP-degrading enzyme ENPP1 allows microglia-derived signaling molecules to trigger STING-dependent inflammation across multiple brain cell types.
bioRxiv · R. Carvalho D et al.
Directly converted human neuronal spheroids preserve donor age and model Alzheimer disease
The three-dimensional cell platform maintains biological aging markers while spontaneously developing hallmark pathologies of sporadic Alzheimer disease.
bioRxiv · Alsolami S et al.
Auditory nerve myelin degeneration defines a subtype of age-related hearing loss
Researchers linked poor auditory nerve synchrony and myelin degradation to amplified communication difficulties in older humans, beyond standard hearing thresholds.
medRxiv : the preprint server for health sciences · Harris KC et al.