# Role of lipocalin-2 in amyotrophic lateral sclerosis

## TL;DR

Lipocalin-2 (LCN2) is linked to ALS progression through inflammation, iron imbalance, and cell death, suggesting it could be a key biomarker and treatment target.

## Contribution

This paper highlights LCN2's role in connecting central and peripheral mechanisms in ALS and proposes it as a promising therapeutic target.

## Key findings

- LCN2 is elevated in ALS patients' blood and tissues.
- LCN2 is involved in neuroinflammation and iron dysregulation in ALS.
- LCN2 is a potential biomarker and therapeutic target for ALS.

## Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized pathologically by degeneration of upper and lower motor neurons, ultimately leading to muscle weakness and respiratory failure. Lipocalin-2 (LCN2) is a secreted protein involved in lipid transport that plays a key role in inflammatory responses and the regulation of iron homeostasis. The role of LCN2 in ALS has attracted increasing attention, as significantly elevated LCN2 expression has been observed in the blood and postmortem tissues of ALS patients. Functionally, LCN2 participates in neuroinflammation, iron dysregulation, cell death, and peripheral immune immunity, proposing a central-peripheral linkage hypothesis mediated by LCN2. Clinically, LCN2 shows promise as both a biomarker and a therapeutic target, with multiple strategies demonstrating potential to mitigate ALS pathology. Moving forward, it is essential to integrate multi-omics to deeply decipher LCN2-mediated molecular networks, advance patient stratification, and accelerate its clinical translation.