Перегляд вихідного коду сторінки Who Else Can I Follow? ALOX15 Fanatics Regarding Facebook

, 2008?and?Kurowska et?al., 2011). In these studies, the authors used immunolabeling for DAT and subsequent light [http://en.wikipedia.org/wiki/ALOX15 ALOX15] microscopy. Surprisingly, in older grafts, these studies described only the expression of DAT in the grafted cell soma, with no reported analysis or discussion of the expression and localization of DAT in the dopamine neuron fibers reinnervating the putamen. In the current study, we also noted a qualitative reduction in the intensity of the DAT signal in the cell soma of the grafted dopamine neurons over time when we compared grafts at 4, 9, and 14 years posttransplantation, but it was striking to us that the punctate DAT expression in the reinnervated putamen and caudate was maintained, even over a decade posttransplantation. We previously showed that the extent of DAT labeling in the caudate and putamen of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys, as detected by [11C]CFT PET neuroimaging, is congruent with the number of surviving dopaminergic fibers (Hantraye et?al., 1992). DAT is a marker of mature dopamine synapse function, and thus our findings of robust DAT labeling in the putamen of patients analyzed in our series are indicative of the long-term, continued health and function of transplanted dopamine neurons. Therefore, based on DAT expression, we do not find evidence of PD pathophysiological processes in grafted dopaminergic neurons. Clearly, using the current transplantation methodology, fetal grafts can result in dopamine neurons that are clinically functional for the long term (Barker et?al., 2013?and?Mendez [http://www.selleckchem.com/products/wnt-c59-c59.html C59 wnt order] et?al., 2005). A previous analysis of ��-synuclein pathology in the same transplant cases described here (Cooper et?al., 2009?and?Mendez et?al., 2008) revealed only one Lewy body in a neuron of a fetal graft in one of these cases (Cooper et?al., 2009). In fetal ventral mesencephalic transplant cases from other transplant-method series, in which we have also observed more frequent Lewy body and ��-synuclein pathology (albeit still [http://www.selleckchem.com/products/MLN8237.html Selleck Alisertib] it was also reported that there is no alteration in the expression of VMAT2, another marker of dopamine presynaptic nerve terminals, in grafted dopamine neurons over time (Kordower et?al., 2008). The current study provides important additional evidence against the relevance of a postulated prion-like ��-synuclein mechanism for disease propagation. Instead of the concept of ��-synuclein spreading from host to graft to cause dysfunction, the opposite may be true, i.e., the healthy transplanted cells provide a clearance mechanism for exogenous unfolded proteins. Our present study unequivocally demonstrates positive markers of dopamine neuron function and thus provides a further rationale for clinical cell therapy for PD using stem cell-derived dopamine neuron equivalents.