Rinsho Shinkeigaku (Clinical Neurology)

The 44th Annual Meeting of the Japanese Society of Neurology

Symposium 8-3: Mlecular mechanism of brain infarction

Masayasu Matsumoto, M.D.1), Hiroshi Yamashita, M.D.1), Kazuo Kitagawa, M.D.2) and Tatsuo Kohriyama, M.D.1)

1)Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical Sciences
2)Department of Internal Medicine and Therapeutics and Department of Clinical Neuroscience, Osaka University Graduate School of Medicine

Through many experimental brain ischemia studies, it has been suggested that all of the cellular elements in the central nervous system show dynamic stress responses depending on the degree of environmental changes induced by ischemia and reperfusion. In this symposium, first we reviewed the pathogenic role of microvascular stasis (i.e., secondary ischemia) caused by the primary ischemic event and demonstrated the important role of cell adhesion molecules through the experiments using ICAM-1 knock-out mouse as a model of brain ischemia/reperfusion. Next, we discussed the ischemia-induced neuronal cell responses in relation to the apoptosis-like selective neuronal death and the induction of adopted stress responses including stress protein synthesis and'ischemic tolerance' phenomenon. A variety of stress proteins induced by ischemic stress have been reviewed in relation to their pathophysiological roles in the ischemic brain. Finally, we reviewed the important pathogenic roles of endoplasmic reticulum (ER) stress as well as adaptive responses of ubiquitin-proteasome system in ischemia-induced neuronal cell death. For the development of a novel therapeutic agent against ischemic stroke, it is quite important to clarify both the negative and positive cellular responses induced by brain ischemia/reperfusion.

(CLINICA NEUROL, 43: 891－893, 2003)
key words: microcirculation, oxidative stress, apoptosis, stress protein, endoplasmic reticulum stress

(Received: 17-May-03)