How are monoclonal antibodies (mAbs) used in neurology classified?

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Classification of Monoclonal Antibodies Used in Neurology

Primary Classification Framework

Monoclonal antibodies in neurology are classified into three main categories based on their mechanism of action: (1) agents targeting leukocyte migration into the CNS, (2) cytolytic antibodies that deplete specific immune cell populations, and (3) antibodies targeting cytokines, chemokines, and their receptors. 1


Category 1: Leukocyte Migration Inhibitors

  • Natalizumab is the prototypical agent in this category, blocking α4-integrin to prevent leukocyte trafficking across the blood-brain barrier into the CNS 1, 2
  • This mechanism directly reduces inflammatory cell infiltration into neural tissue, making it highly effective for relapsing forms of multiple sclerosis 2
  • Natalizumab was the first monoclonal antibody approved for MS treatment and represents a major therapeutic achievement 3

Category 2: Cytolytic (Cell-Depleting) Antibodies

CD20-Targeting Agents (B-Cell Depletion)

  • Rituximab, ocrelizumab, and ofatumumab target CD20-expressing B-cells, causing direct B-cell depletion through antibody-dependent cellular cytotoxicity and complement-mediated lysis 1
  • Ocrelizumab is a recombinant humanized IgG1 monoclonal antibody with a molecular mass of approximately 145 kDa that specifically targets CD20 4
  • These agents eliminate pathogenic B-cells that contribute to autoimmune inflammation in MS 1

CD52-Targeting Agents (Broad Immune Cell Depletion)

  • Alemtuzumab targets CD52, causing profound and prolonged depletion of both T-cells and B-cells 1, 2
  • This produces more extensive immunosuppression compared to selective B-cell depletion, with both greater efficacy and higher risk of secondary autoimmunity 2

Category 3: Cytokine/Chemokine Pathway Modulators

  • Daclizumab targets the IL-2 receptor (CD25), modulating T-cell activation and expansion 1, 2
  • Ustekinumab blocks IL-12 and IL-23 pathways by targeting their shared p40 subunit 1
  • Atacicept and tabalumab target B-cell activating factors (BAFF/APRIL pathways) to reduce B-cell survival and antibody production 1
  • Secukinumab targets IL-17A, blocking pro-inflammatory cytokine signaling 1

Alternative Classification: By Antibody Structure

Structural Nomenclature System

  • The suffix "-mab" indicates monoclonal antibody, with preceding letters denoting the antibody's origin and target 5
  • "-ximab" indicates chimeric antibodies (part mouse, part human protein) 5
  • "-zumab" indicates humanized antibodies (predominantly human with small mouse-derived regions) 5
  • "-umab" indicates fully human antibodies 5

Clinical Implications of Structure

  • Humanized and fully human antibodies have lower immunogenicity risk compared to chimeric antibodies, reducing the likelihood of neutralizing antibody formation 5
  • The degree of humanization affects both efficacy duration and safety profile, with more humanized forms generally better tolerated 5

Distinction from Neuronal Antibodies (Critical Pitfall)

Therapeutic vs. Pathogenic Antibodies

  • Therapeutic monoclonal antibodies (natalizumab, ocrelizumab, etc.) are administered as treatment to modulate immune function 1
  • Neuronal surface antibodies (NMDAR, LGI1, CASPR2, etc.) are pathogenic autoantibodies detected in patients that cause autoimmune neurological syndromes 6

Key Distinguishing Features

  • Neuronal surface antibodies target synaptic receptors and are generally pathogenic through antibody-mediated mechanisms (receptor downregulation or complement-mediated damage) 6
  • Onconeural antibodies (Hu, Ri, Ma2, amphiphysin) target intracellular antigens and serve as markers for paraneoplastic syndromes, with T-cell cytotoxicity as the primary pathogenic mechanism 6
  • GAD antibodies target intracellular glutamic acid decarboxylase but do not generally associate with tumors and are considered markers of immune-mediated syndromes 6

Emerging Applications Beyond Multiple Sclerosis

  • Monoclonal antibodies targeting CGRP (calcitonin gene-related peptide) represent a major breakthrough for migraine prevention, expanding the therapeutic scope of antibodies in neurology 3
  • Experimental antibodies targeting misfolded proteins (amyloid-beta, tau) are in development for neurodegenerative diseases 3
  • Antibodies blocking axonal growth inhibitors (Nogo-A, LINGO-1) are being investigated to promote neural repair and remyelination 3

Clinical Considerations for Neurologists

Target Specificity and Mechanism

  • Monoclonal antibodies offer exceptional target specificity, minimizing non-specific effects compared to traditional immunosuppressants 5
  • However, this specificity means each antibody has distinct class-specific and target-associated risks that must be understood 5

Blood-Brain Barrier Limitations

  • A major challenge for therapeutic antibodies in neurology is their limited access to the brain parenchyma due to the blood-brain barrier 3
  • This limitation is less relevant for antibodies targeting peripheral immune cells (like natalizumab blocking migration) versus those requiring CNS penetration 3

Monitoring Requirements

  • Unlike pathogenic neuronal antibodies where serial antibody levels can guide treatment response, there is no role for repeated measurement of therapeutic monoclonal antibody levels in routine practice 7
  • Clinical and radiographic monitoring remains the standard for assessing therapeutic efficacy 8

References

Research

[Monoclonal antibodies in neurology].

Medecine sciences : M/S, 2019

Research

Monoclonal Antibodies as Neurological Therapeutics.

Pharmaceuticals (Basel, Switzerland), 2021

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Clinical Significance of Glutamic Acid Decarboxylase (GAD) Autoantibodies

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Research

Monoclonal Antibodies: What the Diagnostic Neuroradiologist Needs to Know.

AJNR. American journal of neuroradiology, 2023

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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