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Topic: The Role of Inflammation in Cerebral Aneurysm



           Cerebral aneurysms and inflammation


           Toshihiro Yokoi, Makoto Saito, Yayoi Yoshimura, Keiichi Tsuji, Kazuhiko Nozaki
           Department of Neurosurgery, Shiga University of Medical Science, Shiga 520‑2192, Japan.



                                                   ABSTRA CT
            Multiple  inflammatory  factors,  playing  a  crucial  role  in  cerebral  aneurysm  formation,  have  been  identified.  Tumor  necrosis
            factor‑alpha (TNF‑α) has been revealed to have a close connection with several risk factors that affect aneurysm formation. Remarkable
            expression in aneurysm walls of mRNA for TNF‑α has been observed in humans. Possible therapeutic interventions to reduce the
            formation of cerebral aneurysms may include the inhibition of mediators of inflammation.
            Key words: Cerebral aneurysm, inflammation, molecular biology



           INTRODUCTION                                       size categories. In one study, the annual rupture
                                                              rate of unruptured cerebral aneurysms in a Japanese
           Most unruptured aneurysms, which are detected      cohort was 0.95%.  In another, the average annual
                                                                                [2]
           incidentally show stable clinical courses, exhibit   risk of rupture associated with small unruptured
           fewer inflammatory or degenerative changes in the   aneurysms was 0.54% overall, 0.34% for single
           walls of affected blood vessels, and have a low risk   aneurysms and 0.95% for multiple aneurysms.  The
                                                                                                         [3]
           of rupture. However, some unruptured aneurysms     molecular mechanisms leading to the occurrence,
           show significant changes in size and shape, and the   development, and rupture of cerebral aneurysms
           rupture risk seems to be high. These aneurysms may   have been experimentally investigated. Ruptured
           rupture in the early phase of development or enlarge   aneurysms manifest significant endothelial damage,
           in a short time due to thinning of vessel walls resulting   structural changes in vessel walls, and inflammatory
           from the advancement of degenerative changes. It is of   cell invasion compared to unruptured aneurysms.
                                                                                                             [4]
           clinical relevance to accurately estimate the rupture   The walls of ruptured aneurysms are fragile, possibly
           risk of cerebral aneurysms, but no definitive methods   because macrophage infiltration into the aneurysm
           exist to distinguish rupture‑prone aneurysms from   wall results in the loss of smooth muscle cells and
           rupture‑resistant ones. Recently, the rupture risk of   degeneration of matrix proteins. In this manuscript,
           unruptured cerebral aneurysms was reported. The    we discuss the molecular mechanisms of cerebral
           5‑year cumulative rupture rates for aneurysms located   aneurysm development, focusing on inflammatory
           in the internal carotid artery, anterior communicating   processes.
           artery, anterior cerebral artery, or middle cerebral
           artery in patients without a history of subarachnoid   INFLAMMATION AND ABDOMINAL AORTIC
           hemorrhage were 0%, 2.6%, 14.5%, and 40% for       ANEURYSMS
           aneurysms < 7 mm, 7‑12 mm, 13‑24 mm, and 25 mm
           or greater, respectively.  By comparison, the rupture   The crucial role of inflammatory reactions can be seen
                                [1]
           rates of aneurysms involving the posterior circulation   in the formation of abdominal aortic aneurysms (AAAs).
           and the posterior communicating artery were 2.5%,   Important histological features of vessel walls with
           14.5%, 18.4%, and 50%, respectively, for the same   AAAs include chronic inflammatory cell infiltration
                                                              of the adventitia and media, elastin fragmentation,
                          Access this article online          degeneration, and attenuation of the media. Collagen
               Quick Response Code:                           in the media and adventitia provides tensile strength
                                    Website:                  to the aortic wall. Collagen synthesis increases during
                                    www.nnjournal.net
                                                              the early stages of aneurysm formation, suggesting a
                                                                            [5]
                                    DOI:                      repair process.  Inflammation‑related mediators in
                                    10.4103/2347-8659.153977   aneurysm growth include matrix‑degrading proteinases,
                                                              proinflammatory cytokines, and chemokines.  In later
                                                                                                      [6]
           Corresponding Author: Dr. Toshihiro Yokoi, Department of Neurosurgery, Shiga University of Medical Science,
           Seta Tsukinowa‑cho, Otsu, Shiga 520‑2192, Japan. E‑mail: tyokoi@belle.shiga‑med.ac.jp



          Neuroimmunol Neuroinflammation | Volume 2 | Issue 2 | April 15, 2015                              55
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