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<p>Behçet’s syndrome (BS) is a chronic multisystemic inflammatory disorder with a heterogeneous clinical course. A severe subset with central nervous system involvement (neuro-Behçet’s syndrome, NBS) carries substantial morbidity. While disease activity often decreases with age, the long-term neurological and cognitive outcomes remain poorly defined. Emerging evidence indicates that vascular insufficiency, chronic inflammation, and central nervous system involvement may contribute to cognitive decline in BS, even in the absence of frank neurological symptoms, suggesting a broader and underrecognized impact on brain function. These processes overlap with mechanisms implicated in age-related cognitive decline and dementia, bringing up the hypothesis that BS may accelerate neurodegenerative trajectories in older adults. However, this population remains underrepresented in research. Clarifying whether BS constitutes an overlooked cause or modifier of late-life cognitive decline is clinically urgent. A coordinated agenda spanning neuropsychology, advanced imaging, and biomarkers can deliver diagnostic pathways and testable prevention/management strategies for aging BS populations.</p>

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Aging in Behçet’s syndrome: an overlooked risk for late-life cognitive impairment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Davide Spinetti,
  • Matilde Massara,
  • Camilla Marrone,
  • Elia Salvador,
  • Emma Pepe,
  • Adele Ravelli,
  • Roberto Padoan,
  • Roberta Ramonda,
  • Chiara Ceolin,
  • Giuseppe Sergi,
  • Daniela Mapelli,
  • Marina De Rui,
  • Maria Devita

摘要

Behçet’s syndrome (BS) is a chronic multisystemic inflammatory disorder with a heterogeneous clinical course. A severe subset with central nervous system involvement (neuro-Behçet’s syndrome, NBS) carries substantial morbidity. While disease activity often decreases with age, the long-term neurological and cognitive outcomes remain poorly defined. Emerging evidence indicates that vascular insufficiency, chronic inflammation, and central nervous system involvement may contribute to cognitive decline in BS, even in the absence of frank neurological symptoms, suggesting a broader and underrecognized impact on brain function. These processes overlap with mechanisms implicated in age-related cognitive decline and dementia, bringing up the hypothesis that BS may accelerate neurodegenerative trajectories in older adults. However, this population remains underrepresented in research. Clarifying whether BS constitutes an overlooked cause or modifier of late-life cognitive decline is clinically urgent. A coordinated agenda spanning neuropsychology, advanced imaging, and biomarkers can deliver diagnostic pathways and testable prevention/management strategies for aging BS populations.