LCN2 of cerebrospinal fluid: A potential biomarker for diagnosis and disease progression in Alzheimer's disease

Abstract

Background

Alzheimer's disease (AD) is a neurodegenerative disorder with complex pathological features and pathogenesis, involving aspects such as amyloid-β (Aβ) deposition and neuroinflammation. AD lacks the specific biomarkers for diagnosis, which restricts diagnosis. Recent studies have indicated that Lipocalin-2 (LCN2) plays a direct or indirect role in the occurrence and development of AD. However, whether LCN2 can serve as a biomarker for AD diagnosis remains unclear.

Objective

This study aims to investigate the role of LCN2 in AD and its potential as a biomarker for diagnosis from a clinical perspective.

Methods

We analyze the participant demographic information, LCN2 and Aβ₄₂ levels in cerebrospinal fluid (CSF), and cortex thickness from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database with Welch ANOVA, Linear regression models and other statistical methods.

Results

LCN2 levels in the CSF of AD patients were significantly higher than those in individuals with mild cognitive impairment and no cognitive impairment. The LCN2 levels were closely associated with cognitive decline and pathological features of AD, including Aβ deposition, and reduced cortical thickness, but no tau protein phosphorylation. Age was an important confounding factor affecting the relationship between LCN2 and Aβ₄₂, while gender, years of education, and APOE carrier status did not have a significant impact. Furthermore, LCN2 was linked to the upregulation of inflammatory markers, indicating its potential involvement in the neuroinflammatory processes of AD.

Conclusions

LCN2 is not only a potential biomarker for the early diagnosis of AD but may also play a significant role in the neurodegenerative processes associated with the disease.