After a stroke, millions of brain neurons die within minutes. While the dead cells can’t be restored, some tissue around the dead area remains alive but non-functioning. Research has found that cell therapy target the area with growth factors that save and rejuvenate that tissue.

Infarction causes an acute loss of different cells such as neurons and glial cells in the brain. The only neuroprotective agent developed for stroke in clinical use is recombinant tissue plasminogen activator (rtPA), which is employed for thrombolysis and has a therapeutic window of merely 3–4.5 h. There is thus a compelling need to develop therapeutic agents that extend beyond the first few hours after onset of stroke. This requires a paradigm shift to the usage of new strategies from neuroprotection to neuro-restoration that treat the injured or compromised brain tissue.

Cell therapy has the capacity to differentiate into all types of cells. Exogenously administered cells appear to stimulate endogenous reparative processes and do not replace injured cerebral tissue. It was once thought that intravenously administered cells would home in on the injured site and replace the dead neurons, but the current ideology for the use of these cells holds that these cells release many trophic factors like VEGF, IGF, BDNF and tissue growth factors that stimulate brain plasticity and recovery mechanisms. Up regulation of growth factors, prevention of ongoing cell death, and enhancement of synaptic connectivity between the host and graft are some of the common pathways through which intravenous stem cells work as “chaperones.