# Structure and function of the blood–brain barrier in perioperative neurocognitive disorders

**Authors:** Yipeng Su, Yiting Chen, Bingqi Zheng, Yiting Huang, Zhongxiao Liao, Xiaochun Zheng, Fei Gao

PMC · DOI: 10.3389/fnins.2025.1690354 · 2026-01-02

## TL;DR

This paper reviews how changes in the blood-brain barrier may contribute to cognitive disorders in elderly patients after surgery, aiming to find new treatment approaches.

## Contribution

The paper integrates recent findings on blood-brain barrier changes in PNDs to propose novel preventive and therapeutic strategies.

## Key findings

- Damage to the blood-brain barrier is a critical factor in the development of perioperative neurocognitive disorders.
- Multiple mechanisms like neuroinflammation and Aβ deposition are linked to BBB dysfunction in PNDs.
- Understanding BBB changes could lead to new prevention and treatment strategies for PNDs.

## Abstract

Perioperative neurocognitive disorders (PNDs) are the most common neurological complications in elderly patients undergoing surgery. Patients with PNDs have significantly greater incidences of postoperative disability and mortality. Currently, there are no specific treatments for PNDs.

This review integrates the latest evidence examining the role of structural and functional changes in the blood–brain barrier (BBB) in the pathological mechanisms of PNDs, with the aim of identifying innovative preventive strategies and promising therapeutic targets for PNDs.

Researchers have proposed various hypotheses to shed light on the pathogenesis of PNDs, including neuroinflammation, neurotransmitter or receptor abnormalities, beta-amyloid (Aβ) deposition and tau protein phosphorylation, oxidative stress, iron homeostasis imbalance, circadian rhythm disruption, and changes in the gut microbiota. Damage to the BBB plays a critical role in the pathogenesis of PNDs.

This article summarizes the role of BBB structural and functional changes in the pathogenesis of PNDs reported in recent studies, with the goal of providing new ideas for preventing and treating PNDs.

## Full-text entities

- **Genes:** MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}
- **Diseases:** PNDs (MESH:D019965), neurological complications (MESH:D002493), neuroinflammation (MESH:D000090862), postoperative disability (MESH:D019106)
- **Chemicals:** iron (MESH:D007501)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12824458/full.md

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Source: https://tomesphere.com/paper/PMC12824458