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The occurrence of striatal neurogenesis after stroke, focuses the interest on individuals with basal ganglia infarcts.If stem cells can also generate cortical neurons and repair axonal damage, individuals with lesions in the cerebral cortex may be included.A strategy for repair of Spermine infarcted white matter was suggested recently by the observation that NEUROSPHERES derived from adult tissue injected intravenously or intraventricularly in mice gave rise to cells that migrated to demyelinated areas and remyelinated axons.Muscle weakness progresses rapidly and causes death within N EUROD EG EN ER AT ION JU LY S R E V I E W a few years.To have longterm value, stem cell therapy must restore function of both upper and lower motor neurons.Successful replacement of cortical motor neurons requires not only reestablishment of spinal cord connections but also precise functional integration of the new neurons into cortical circuitries.Corticospinal or corticobulbar systems are not reconstructed after implantation of fetal cortical tissue into adult neocortex.Latestage fetal cortical neurons, however, replace apoptotic neurons when grafted into adult mouse neocortex, receive afferents from host brain and project to the contralateral hemisphere.This finding supports the strategy of differentiating stem cells along specific cortical neuronal lineages in vitro and transplanting them so as to reconstruct cortical circuitry.It is unknown, though, if such cortical neuronal replacement will work in the brains of individuals with ALS.Whether these neurons are integrated in neuronal circuits and restore reflexes and voluntary movements is unclear.Functional benefits have been detected after cell implantation in ALS models, although it is unlikely that the observed effects were due to neuronal replacement and reestablishment of connectivity.Spinal grafts of neurons generated from the human NT cell line and intravenous administration of human umbilical cord blood cells Furosemide delayed disease progression in mice.Human embryonic germ cell derivatives delivered into the CSF of rats with motor neuron injury were distributed over the spinal cord and migrated into the parenchyma.The paralyzed rats showed partial motor recovery, probably because the grafted cells protected host neurons and facilitated their reafferentation by secreting growth factors.A great deal of basic research should be done before persons with ALS should be considered for clinical trials.Cells with characteristics of cholinergic neurons have been generated from stem cells of various sources, but their functional properties and ability to repair the spinal cord in ALS models are unknown.In the shorter term, strategies to retard disease progression seem to be a more realistic clinical approach as compared with neuronal replacement.The main pathology is a loss of medium spiny projection neurons in the striatum due to a mutation in the huntingtin gene.In animal models, intrastriatal grafts of fetal striatal tissue containing projection neurons reestablish connections with the globus pallidus and receive inputs from host cerebral cortex.This level of reconstruction of corticostriatopallidal circuitry is sufficient to reverse motor and cognitive deficits in rats and monkeys.The grafts survived without typical pathology, contained striatal projection neurons and interneurons, and received afferents from the patients brain.However, the extent of clinical benefit was unclear.One openlabel trial indicated cognitive and motor improvements, whereas outcome was unchanged in the other.

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