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Related Experiment Video

Updated: May 28, 2026

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Inflammation in Aneurysmal Subarachnoid Hemorrhage: Cause, Consequence, or Both? Focus on Pathogen Pattern

Juhana Frösén1,2,3, Pervinder Bhogal4

  • 1Department of Clinical Medicine, Hemorrhagic Brain Pathology Research Group, Faculty of Medicine and Health Technology, Tampere University, Finland (J.F.).

Stroke
|May 27, 2026
PubMed
Summary

Pattern recognition receptors (PPRs) and their ligands, pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), drive inflammation in intracranial aneurysms. Targeting these pathways may prevent rupture and subsequent hemorrhage.

Keywords:
immunity, innateinflammationintracranial aneurysmpathogen-associated molecular pattern moleculessubarachnoid hemorrhage

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Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Inflammation is critical in intracranial aneurysm (IA) development, progression, and rupture, leading to aneurysmal subarachnoid hemorrhage (aSAH).
  • Pattern recognition receptors (PPRs) mediate innate immunity, responding to microbial and non-microbial danger signals.

Purpose of the Study:

  • To review the role of PPRs, PAMPs, and DAMPs in IA pathogenesis and aSAH-induced neuronal injury.
  • To explore potential therapeutic strategies targeting these inflammatory pathways.

Main Methods:

  • Narrative review of existing literature on PPRs, PAMPs, DAMPs, and intracranial aneurysms.
  • Analysis of the inflammatory mechanisms involved in IA formation, progression, and rupture.
  • Discussion of therapeutic targets for IA and aSAH.

Main Results:

  • PPR activation by PAMPs and DAMPs contributes to excessive inflammation, cell death, and tissue remodeling in IAs.
  • These inflammatory processes are implicated in IA rupture and subsequent neuronal damage following aSAH.

Conclusions:

  • PPRs, PAMPs, and DAMPs are key players in the inflammatory cascade of intracranial aneurysms.
  • Targeting these innate immune mediators offers promising therapeutic avenues to prevent IA rupture and aSAH-related neurological deficits.