For example, at 6 or 7 years after transplantation,
Keene et al.  demonstrated grafted cell survival, as shown by the various striatal markers found within the grafted MAPK inhibitor tissue. However, basic markers of cell cytoarchitecture such as haematoxylin & eosin and Nissl reveal that grafted cells depict a morphology very different from host cells . Cells within p-zones are ballooned, vacuolated, lack structural cytoplasmic integrity and even stain positively for apoptotic markers such as caspase-3. When identical immunohistological stainings are compared between the reports by Keene and Cicchetti, and those published for the 6-  and 18-month post-transplantation cases , it is apparent that grafted striatal projection neurones exhibit a much weaker staining and that they lack dendritic extensions almost completely
[43,45], pointing to a rather unhealthy morphology. In contrast, various subclasses of striatal interneurones including NADPH-d-, ChAT-, parvalbumin- and calretinin-positive cells, show a better long-term survival, suggesting a degeneration or neuronal sparing pattern similar to that observed with HD pathology [42,43,46]. Although there may be signs of degeneration PI3K inhibitor within the grafted tissue, ingrowth of host-derived TH fibres can be observed, suggesting connections and interactions between the host and donor cells [43,46]. These results are in accordance with earlier animal model studies as well as transplanted PD patients [55,56]. Such TH innervation was not found in the 10-year post-transplantation case depicting cysts and mass lesions , suggesting that TH innervation of grafted tissue is not a random process. However, DARPP-32-
and calbindin-positive Dimethyl sulfoxide cells within the grafts do not appear to cross the graft–host interface, suggesting a limited connectivity of the graft with the host brain . One study reported the presence of cortical glutamatergic input onto the grafted striatal cells, using both immunohistochemistry and transmission electron microscopy . Moreover, a notable microglial and astrocytic gliosis was observed in the vicinity of grafted tissue 9–10 years after transplantation [43,44], while such a response was found to be less intense in the graft than in the host at earlier intervals (6 and 7 years) . Finally, elements associated to vasculature and vasculature network, such as endothelial cells and capillaries [stained with Von Willebrand factor (vWF)], pericytes [using platelet derived growth factor receptor-beta (PDGFR-β) as a marker] and larger-calibre blood vessels [detected with the α-smooth muscle actin (α-SMA) marker], demonstrated poor revascularization of the grafted tissue .