The 22nd Princeton Conference on Cerebrovascular Disease, held in Redwood City, California, 10–12 March 2000, was hosted by the Stanford University School of Medicine, with administrative support provided by the Neurosurgical Laboratories, Department of Neurosurgery. The Conference focused on the current status and future directions of stroke pathophysiology, diagnosis and treatment, with special emphasis on the cellular and molecular mechanisms of ischemic cell death and repair, and clinical aspects of imaging, risk factors and therapeutic strategies in stroke. This 2 day conference was exciting and productive, with a consensus that the goals that were set forth for this meeting had been accomplished, and perhaps far exceeded expectations. First, the meeting provided a unique forum for promoting collaborative interaction in stroke research among the attendees. Second, many of the speakers presented state-of-the-art and up-to-date information, and the vigorous interactive discussions among the participants made this conference a successful and memorable one.

The first three topics in this monograph are directed toward the cellular and molecular mechanisms of ischemic cell death. Zinc and caspases, which are emerging as important mediators involved in ischemic cell death, have been fully elaborated in the two special invited lectures. Other important mediators including oxygen radicals, NMDA receptors and genes involved in ischemic tolerance are discussed. Two major concepts, parapoptosis and ischemic white matter injury in culture, are introduced.

One major area that distinguishes this meeting from other stroke conferences is that late-breaking news in stroke research was presented, and appears in this book in Part IV.