# C-Reactive Protein and Neurological Autoimmune Diseases: Bridging the Diagnostic and Pathogenic Gap

## TL;DR

This paper explores how C-reactive protein (CRP) connects systemic inflammation to neurological autoimmune diseases like MS and GBS, highlighting its role in disease progression and outcomes.

## Contribution

The paper provides a comprehensive review of CRP's mechanistic and clinical roles in neuroinflammatory disorders, integrating molecular and clinical perspectives.

## Key findings

- Elevated CRP levels correlate with worse outcomes in diseases like MS and GBS.
- CRP serves as both an effector and reporter of inflammation in neuroautoimmune conditions.
- CRP-based composite indices show promise as prognostic markers but face limitations in specificity.

## Abstract

C-reactive protein (CRP) has emerged as a crucial link between systemic and neuroinflammatory processes, though its role across neurological autoimmune disorders remains incompletely understood. Pathologies such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), Guillain–Barré syndrome (GBS), and myasthenia gravis (MG) share chronic, dysregulated inflammation resulting from loss of immune tolerance. Their pathogenesis arises from interactions among genetic susceptibility, environmental factors, and gut microbiota alterations that trigger autoreactive immune cascades through molecular mimicry, ectopic antigen expression, or paraneoplastic cross-reactivity. These immune pathways sustain inflammation and promote neuroaxonal injury. CRP, synthesized mainly by hepatocytes in response to interleukin-6 (IL-6), functions as both an effector and reporter of inflammation, linking systemic immune activation to neuroinflammatory damage. Elevated CRP levels correlate with unfavorable outcomes, including accelerated disability in MS, IL-6-mediated astrocyte injury in NMOSD, respiratory failure in GBS, and crisis susceptibility in MG. Composite indices such as the CRP-to-albumin ratio are emerging as refined prognostic markers, though interpretation is limited by non-specificity and biological variability. This review integrates current evidence on CRP’s mechanistic roles, clinical associations, and translational potential in neuroinflammatory disorders, combining molecular, clinical, and imaging perspectives to refine its role within inflammation-driven neurodegeneration.