Yetimler, Berrak

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Job Title:Dr. Öğr. Üyesi
Email Address:berrak.yetimler@agu.edu.tr
Main Affiliation:04.02. Moleküler Biyoloji ve Genetik
Status: Current Staff
ORCID:ORCID Profile0000-0003-2807-4194
Scopus ID:Scopus Profile55342957000
YÖK Akademik: 741F54449CDC13D5
Google Scholar:Google Scholar ProfilekEHkReQAAAAJ&hl
Web of Science ID:Web of Science ProfileLZE-2698-2025
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Berrak Yetimler
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Author of Publication: search.filters.isAuthorOfPublication.3ba8952f-5fe0-4ae3-816f-2c46f14cd3e9

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  • Article
    Immune-Driven Mechanisms in Idiopathic Intracranial Hypertension: A Critical Synthesis
    (Walter de Gruyter GmbH, 2026) Tuzun, Erdem; Yetimler, Berrak
    Idiopathic intracranial hypertension (IIH) is increasingly recognised as a complex disorder characterized by elevated intracranial pressure (ICP), with evidence suggesting contributions from dysregulated cerebrospinal fluid (CSF) dynamics as well as metabolic, endocrine, and neurovascular mechanisms. IIH predominantly affects women of reproductive age who are living with obesity. Clinically, IIH may be asymptomatic or present with severe headaches, visual disturbances, and papilledema, with a risk of visual impairment in some untreated or refractory cases. Although the etiopathogenesis of IIH remains unclear, emerging evidence from metabolic and immunological studies suggests that immune-mediated mechanisms may contribute to disease pathophysiology. In this review, we synthesize current literature on the potential contribution of the immune system to IIH, integrating findings across obesity-associated inflammation, circulating cytokine profiles, comorbid inflammatory and autoimmune conditions, and markers of neuroglial stress and injury. We summarize converging data suggesting that IIH may, at least in part, be influenced by a pro-inflammatory milieu that affects CSF dynamics. While available studies highlight intriguing immunological signals, the underlying mechanistic pathways remain poorly resolved. Larger, longitudinal, and mechanistically grounded investigations are needed to clarify causality, identify relevant immune subtypes, and determine whether immune modulation may offer therapeutic opportunities in IIH.

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