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. These hot topics include the gap junction between astrocytes, the aquaporin-
4 water channel, tetracycline neuroprotection and spreading depression.
Postischemic pathophysiological events are discussed in Parts V and VI.
Hemorrhage and inflammation are two major areas of focus. New concepts in the
role of thrombolytic tissue plasminogen activator and cytokines in postischemic
pathophysiology and injury have evolved from these presentations.
Parts VII and VIII focus on the preclinical utility of gene transfer in stroke, and
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neural stem cell transplantation and its involvement in neural plasticity after cerebral
ischemia. These studies present up-to-date and unique therapeutic strategies
and potentials employing gene transfer and stem cells in clinical stroke.
Diffusion/perfusion magnetic resonance imaging in clinical stroke dominate the
discussions in Part IX. New and innovative approaches using these imaging techniques
in addressing acute ischemic stroke, transient ischemic attack and early
recanalization in acute ischemic stroke have been vigorously discussed and
debated.
Finally, a particular section (Part X) is devoted to risk factors, clinical trials and
new therapeutic horizons. This section presents a unique perspective for considering
vascular factors and white matter as the new neuroprotection targets in stroke
clinical trials.
The enthusiasm and excitement reflected in the presentations and the vigorous
interactive discussions among the participants reflect the success of the conference.
This momentum is likely to continue. Tremendous advances in both basic and clinical
sciences were demonstrated during the 2 day meeting. It is our hope that these
advances, as communicated through this volume, will provide an impetus for
stroke researchers to maintain and exceed these excitements in advancing our
knowledge in both the basic and clinical sciences of stroke.
Cerebrovascular Disease