Neuronal cell death occurs extensively during development and pathology, where it is
especially important because of the limited capacity of adult neurons to proliferate or be …

Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from
a complex series of pathophysiological events that evolve in time and space. In this article …

Poly (ADP-ribose) polymerase 1 (PARP1) is a nuclear protein that is activated by binding to
DNA lesions and catalyzes poly (ADP-ribosyl) ation of nuclear acceptor proteins, including …

This review is directed at understanding how neuronal death occurs in two distinct insults,
global ischemia and focal ischemia. These are the two principal rodent models for human …

Background and Purpose—Traditionally, cell death after cerebral ischemia was considered
to be exclusively necrotic in nature, but research over the past decade has revealed that …

Over the past two decades, research has heavily emphasized basic mechanisms that
irreversibly damage brain cells after stroke. Much attention has focused on what makes …

Caspases play an essential role during apoptotic cell death. These enzymes define a new
class of cysteine proteases and comprise a multi-gene family with more than a dozen distinct …

A form of cell death called apoptosis is a prominent feature in a broad spectrum of
neurodegenerative diseases, ranging from stroke to Huntington's disease. Hypoxia, toxic …

Neuronal death in cerebral ischemia is largely due to excitotoxic mechanisms, which are
known to activate the c-Jun N-terminal kinase (JNK) pathway. We have evaluated the …

Background—Neuroprotective drugs for acute stroke have appeared to work in animals,
only to fail when tested in humans. With the failure of so many clinical trials, the future of …