Mitochondrial dysfunction in postoperative cognitive dysfunction: From preclinical mechanisms to multimodal...

Area of Science:

• Neuroscience
• Cell Biology
• Pathology

Background:

• Postoperative cognitive dysfunction (POCD) is a significant clinical issue impacting patient recovery.
• Mitochondrial dysfunction is increasingly recognized as a key factor in POCD development.
• Understanding the molecular mechanisms is crucial for effective interventions.

Purpose of the Study:

• To review the central role of mitochondrial dysfunction in POCD pathogenesis.
• To elucidate key molecular pathways linking mitochondria to cognitive decline after surgery.
• To synthesize recent advances in diagnostic and preventive strategies targeting mitochondria in POCD.

Main Methods:

• Literature review of mechanistic pathways involving mitochondria in POCD.
• Analysis of bioenergetic, oxidative stress, calcium signaling, and quality control mechanisms.
• Synthesis of preclinical and clinical research on mitochondria-targeted interventions.

Main Results:

• Mitochondrial dysfunction involves bioenergetic impairment, oxidative stress, neuroinflammation, calcium dysregulation, and defective quality control (mitophagy, genetic integrity).
• These pathways collectively contribute to cognitive decline observed in POCD.
• Recent advances highlight potential diagnostic and preventive strategies.

Conclusions:

• Mitochondrial dysfunction is a critical pathogenic factor in POCD.
• Targeting specific mitochondrial pathways presents a promising avenue for POCD diagnostics and therapeutics.
• Further translational research is needed to bridge basic science discoveries with clinical applications.