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(Stroke. 2003;34:2082.)
© 2003 American Heart Association, Inc.

Controversies in Stroke

Stem Cells: Do They Replace or Stimulate?

From the University of Melbourne and National Stroke Research Institute, Austin & Repatriation Medical Centre, Melbourne, Australia.

Correspondence to Dr David Howells, University of Melbourne and National Stroke Research Institute, Austin & Repatriation Medical Center, Level 7, Department of Medicine, Heidelberg, Victoria 3084, Australia. E-mail david.howells@unimelb.edu.au

Key Words: regeneration • stem cells • transplantation

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

In 2002, more than 6000 articles were published on stem cell biology. Many argued that the importance of these cells lies in their potential to provide transplants for treatment of diseases such as stroke, Parkinson’s disease, and spinal cord injury. The fervor is such that human embryos have been cloned, despite substantial ethical concerns, with the justification that "therapeutic cloning" will provide the stem cells needed for widespread transplantation for incurable diseases.

Stem cells prepared from human bone marrow,¹ neuronal progenitor cells from adult rat dentate gyrus,² and embryonic human forebrain³ all engraft successfully within the brain parenchyma and can differentiate into neurons.² Surprisingly these engrafted cells can migrate to join existing neural stem cell migratory pathways,^1,3 and when the brain is injured, migration is redirected specifically to the site of damage.⁴

After stroke in rodents, stem cells derived from bone marrow induce functional recovery measured by rotarod, adhesive-removal, and modified neurologic severity score tests when implanted into striatum⁵ or cortex⁶ or after intra-arterial infusion.⁷ Importantly, these improvements were noted when implantation occurred up to 14 days⁷ after stroke, were enhanced by brain-derived neurotrophic factor,⁸ and were achieved when very few implanted cells expressed neural markers⁹ and still retained a relatively undifferentiated morphology.⁶ Importantly, despite marked functional improvements, the infarcts do not get smaller.⁵ This latter observation would appear to exclude the possibility that the stem cells secrete neuroprotective factors that enhance survival of neurons susceptible to infarction.

These observations have led to speculation that increased host plasticity rather than . . . [Full Text of this Article]