Cortical plasticity in AQP4-positive NMOSD: a transcranial magnetic stimulation study

Cereb Cortex. 2024 Aug 1;34(8):bhae345. doi: 10.1093/cercor/bhae345.

Abstract

Aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) is an autoimmune disease characterized by suboptimal recovery from attacks and long-term disability. Experimental data suggest that AQP4 antibodies can disrupt neuroplasticity, a fundamental driver of brain recovery. A well-established method to assess brain LTP is through intermittent theta-burst stimulation (iTBS). This study aimed to explore neuroplasticity in AQP4-NMOSD patients by examining long-term potentiation (LTP) through iTBS. We conducted a proof-of-principle study including 8 patients with AQP4-NMOSD, 8 patients with multiple sclerosis (MS), and 8 healthy controls (HC) in which iTBS was administered to induce LTP-like effects. iTBS-induced LTP exhibited significant differences among the 3 groups (p: 0.006). Notably, AQP4-NMOSD patients demonstrated impaired plasticity compared to both HC (p = 0.01) and pwMS (p = 0.02). This pilot study provides the first in vivo evidence supporting impaired neuroplasticity in AQP4-NMOSD patients. Impaired cortical plasticity may hinder recovery following attacks suggesting a need for targeted rehabilitation strategies.

Keywords: Itbs; Ltp; Tms; demyelinating disease; neurophysiology.

MeSH terms

  • Adult
  • Aquaporin 4* / immunology
  • Aquaporin 4* / metabolism
  • Autoantibodies / immunology
  • Cerebral Cortex / physiology
  • Female
  • Humans
  • Long-Term Potentiation / physiology
  • Male
  • Middle Aged
  • Neuromyelitis Optica* / immunology
  • Neuromyelitis Optica* / physiopathology
  • Neuronal Plasticity / physiology
  • Pilot Projects
  • Transcranial Magnetic Stimulation* / methods

Substances

  • Aquaporin 4
  • AQP4 protein, human
  • Autoantibodies