Abstract
The treatment for intracranial aneurysm (IA) is socially important because of poor outcome posed by subarachnoid hemorrhage after rupture. Further, the incidence of IAs in general public is high and, indeed, in developed countries many IAs are incidentally found through brain check. However, to date, options for treatment of IAs to prevent rupture are quite limited only to surgical procedures such as microsurgical clipping and endovascular coiling. Taking into account unavoidable risks of complication from surgical interventions and numerous aneurysm careers without treatment, less invasive medical therapies should be established. In human IA lesions, the presence of inflammatory responses, such as expressions of pro-inflammatory mediators and infiltration of inflammatory cells, have been reported, which suggests the involvement of inflammatory responses in the pathogenesis of IA. Recent experimental studies using rodent models have revealed the crucial role of inflammatory responses mediated by NF-κB activation in IA formation and progression and supported the notion that IA is an inflammatory disease affected intracranial arteries. To find out a candidate drug for IA treatments, the effect of several drugs with anti-inflammatory and anti-NF-κB actions on IA progression has been examined using rodent models and revealed the excellent inhibitory effect of statins (HMG-CoA reductase inhibitors) on IA progression. Based on these findings, the case-control study was recently carried out enrolling patients with unruptured or ruptured IAs to examine the effect of statin usage on rupture. This study revealed the significant differences in the ratio of statin usage between two groups and notably the remarkable reduction of risk of rupture of pre-existing IAs under statin usage at the adjusted odds ratio of 0.30. Recent laboratory and clinical studies make considerable achievement toward the future development of drugs for IA treatment and especially suggest the potential of statins as a candidate.
Highlights
Recent advance in medical technology greatly contributes to improving the outcome of various diseases including intracranial diseases
The cause of subarachnoid hemorrhage is, in most cases, rupture of pre-existing intracranial aneurysm (IA), a lesion with regional bulging of intracranial arteries histologically characterized by the disrupted internal elastic lamina and the degeneration of media
We briefly summarize the proposed mechanisms underlying IA formation especially focused on NF-κB-mediated inflammation and discuss its potential as a therapeutic target for treatment
Summary
Recent advance in medical technology greatly contributes to improving the outcome of various diseases including intracranial diseases. Even today, subarachnoid hemorrhage still poses a high risk of mortality and severe morbidity despite intensive treatments [1]. The cause of subarachnoid hemorrhage is, in most cases, rupture of pre-existing intracranial aneurysm (IA), a lesion with regional bulging of intracranial arteries histologically characterized by the disrupted internal elastic lamina and the degeneration of media. Many IAs are incidentally found before rupture through imaging tests by CT or MRI in developed countries. To date, there is no medical treatment available for these incidentally found IAs except for surgical procedures, microsurgical clipping and endovascular coiling, to prevent rupture and resultant subarachnoid hemorrhage [4]-[6]. Considering the social loss due to a resultant subarachnoid hemorrhage after rupture, unavoidable risk of complication in surgical procedures and the high incidence of IAs, a new medical treatment for preventing rupture of pre-existing IAs should be developed. We introduce the future prospection for the development of drugs for IA treatment
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
