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(Stroke. 2003;34:2081.)
© 2003 American Heart Association, Inc.

Controversies in Stroke

Cell Therapy: Replacement

From the Departments of Neurology (L.R.W.) and Neurological Surgery (D.K.), University of Pittsburgh School of Medicine, Pittsburgh, Pa.

Correspondence to Dr Lawrence R. Wechsler, University of Pittsburgh Medical Center, Stroke Institute, Department of Neurology, C426 PUH, 200 Lothrop St, Pittsburgh, PA 15213. E-mail lwechsler@stroke.upmc.edu

Key Words: regeneration • stem cells

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

Not long ago, the ability of the brain to restore function through regeneration of neural elements was thought to be nonexistent. It is now known that not only does some regenerative capacity exist, but implanted cells can integrate into the host brain, survive, and reverse neurological deficits. Neural stem cells, fetal transplants, immortalized cell lines, and bone marrow stromal cells show promise in experimental models of neurological disease including stroke. Although it is clear that transplanted cells function, the mechanism by which neurological deficits might improve is less certain. Transplanted cells may preserve existing host cells and connections through secretion of trophic factors; establish local connections that enhance synaptic activity; provide a bridge for host axonal regeneration; or actually replace cellular elements. Several observations from animal and human studies of cell therapy support the possibility that transplanted cells exert at least some of their effect through cellular replacement.

In the early stages of brain development, implanting neural stem cells leads to replacement of multiple cellular elements including neurons and glia.¹ Thus, the potential for cell replacement exists, but whether it persists into adulthood is uncertain. Models of Parkinson’s disease (PD) provide the most direct support for cell replacement as an important effect of cell therapy. Fetal ventral mesencephalic neurons grafted into the striatum in animal models of PD restore dopamine levels and improve function.² Similar grafts outside the striatum fail to achieve clinical benefit. In humans, such fetal grafts produce clinical benefit³ that accrues gradually rather than immediately, suggesting an . . . [Full Text of this Article]

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