This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Moskowitz, M. A. Articles by Lo, E. H. Search for Related Content PubMed PubMed Citation Articles by Moskowitz, M. A. Articles by Lo, E. H. Pubmed/NCBI databases Medline Plus Health Information Stroke

(Stroke. 2003;34:324.)
© 2003 American Heart Association, Inc.

Advances in Stroke 2002

Neurogenesis and Apoptotic Cell Death

Michael A. Moskowitz, MD Eng H. Lo, PhD

From the Neuroscience Center (M.A.M.) and Neuroprotection Research Laboratory (E.H.L.), Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Mass.

Correspondence to Michael A. Moskowitz, MD, Massachusetts General Hospital, 149 13th St, Rm 6403, Charlestown, MA 02129. E-mail Moskowitz@helix.mgh.harvard.edu

Key Words: apoptosis • caspases • growth factors • neurogenesis • stem cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

As recently as a decade ago, it seemed inconceivable to most neuroscientists that new neurons could be born routinely in the adult mammalian brain (neurogenesis) and that neurons and other brain cells die by committing a form of cell suicide (apoptosis). Both fields have evolved into large research enterprises that continue to revolutionize how we think about limiting cell injury and cell death in the adult brain and spinal cord. Moreover, both have afforded new possibilities that one day may help to restore normal function to the injured nervous system. In fact, this past year’s Nobel prize in Physiology and Medicine was awarded to Robert J. Horvitz of the Massachusetts Institute of Technology for his pioneering experiments elucidating complex pathways promoting and blocking programmed cell death in the nematode C elegans. Horvitz’s elegant discoveries showed how genes and proteins expressed within evolutionarily ancient and biologically less complex organisms can profoundly influence our understanding of cell death in the mammalian nervous system, with equally important implications for the developing brain and for brain cancer. This review examines recent advances underscoring the importance of neurogenesis and neuronal cell death to the adult brain after stroke.

Neurogenesis

Replenishing brain cells from endogenous and exogenous sources is one of the most exciting frontiers in stroke research.^1,2 In normal adult brain, neuroblasts from the subventricular zone (SVZ) migrate via the rostral migratory stream toward the olfactory bulb, whereas neuroblasts from the subgranular layer mostly supply the hippocampus. After transient global ischemia, precursor cells within the . . . [Full Text of this Article]

This article has been cited by other articles:

				M. Lalancette-Hebert, D. Phaneuf, G. Soucy, Y. C. Weng, and J. Kriz Live imaging of Toll-like receptor 2 response in cerebral ischaemia reveals a role of olfactory bulb microglia as modulators of inflammation Brain, April 1, 2009; 132(4): 940 - 954. [Abstract] [Full Text] [PDF]

				J. A. Zivin, G. W. Albers, N. Bornstein, T. Chippendale, B. Dahlof, T. Devlin, M. Fisher, W. Hacke, W. Holt, S. Ilic, et al. Effectiveness and Safety of Transcranial Laser Therapy for Acute Ischemic Stroke Stroke, April 1, 2009; 40(4): 1359 - 1364. [Abstract] [Full Text] [PDF]

				X. Wang, G. Z. Feuerstein, L. Xu, H. Wang, W. A. Schumacher, M. L. Ogletree, R. Taub, J. J.-W. Duan, C. P. Decicco, and R.-Q. Liu Inhibition of Tumor Necrosis Factor-{alpha}-Converting Enzyme by a Selective Antagonist Protects Brain from Focal Ischemic Injury in Rats Mol. Pharmacol., April 1, 2004; 65(4): 890 - 896. [Abstract] [Full Text]