Glymphatic dysfunction as a potential mechanistic link to cognitive ımpairment in Behçet's disease: a hypothesis.

چکیده اصلی

Behçet's disease (BD) is a chronic multisystem inflammatory disease in which cognitive impairment is increasingly recognized but remains incompletely understood. Although cognitive dysfunction is more common in patients with Neuro-Behçet's disease (NBD), it has also been reported in patients without clinically apparent neurological involvement, suggesting that mechanisms beyond focal inflammatory lesions may contribute to cognitive impairment. The glymphatic system is a brain-wide perivascular clearance pathway that maintains cerebral homeostasis by facilitating the exchange of cerebrospinal and interstitial fluid and the removal of inflammatory mediators and metabolic waste products. Previous neuroimaging studies have demonstrated white matter microstructural abnormalities in both NBD and neurologically asymptomatic BD, with more extensive alterations in NBD. Furthermore, studies in systemic lupus erythematosus have identified an increased burden of enlarged perivascular spaces, choroid plexus enlargement, and lower diffusion tensor imaging along the perivascular space (DTI-ALPS) indices, providing preliminary imaging evidence of alterations putatively related to glymphatic function in systemic inflammation and neuropsychiatric involvement. However, the relationship between glymphatic dysfunction and cognitive impairment has not yet been directly investigated in BD. We hypothesize that chronic neuroinflammation, endothelial dysfunction, blood-brain barrier disruption, vascular inflammation, and sleep disturbance may impair glymphatic clearance in BD, leading to persistent neuroinflammation, white matter injury, and cognitive dysfunction. This proposed relationship has not yet been directly tested in BD. We further propose that glymphatic dysfunction may occur not only in patients with NBD but also in a subset of BD patients without overt neurological involvement, although it is likely to be more pronounced in NBD. If validated, this hypothesis could provide a novel mechanistic framework for cognitive impairment in BD and support the development of imaging biomarkers and adjunctive therapeutic strategies targeting glymphatic function.

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