Lewy body–like pathology in long-term embryonic nigral transplants in Parkinson's disease

By J. Kordower, Y. Chu, R. Hauser, T. Freeman, W. Olanow. Nature Medicine, 2008

1,670 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/49118e7682f5442fded572ae34d627d25712bf29

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In Cellular and Molecular Neuroscience

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Citations in the corpus

α-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells. (2011, positive): “Indeed, the initial post-mortem reports on LB and LN in grafted neurons in PD were made in patients who died more than a decade after transplantation (10, 11).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “At autopsy between 10 and 16 years after transplantation, Lewy body pathology was not only observed in the host striatal neurons but also in the grafted neurons of some PD patients (Kordower et al , 2008a, b; Li et al , 2008, 2010; Mendez et al , 2008).”
Prion-like spreading of pathological α-synuclein in brain (2013, background): “Kordower et al. (2008) and Li et al. (2008) reported that embryonic neurons transplanted into the striatum of an individual with Parkinson’s disease developed Lewy body-like pathologies, suggesting that pathological -synuclein may be transmissible from diseased neurons to healthy neurons.”
Parkinson's disease and parkinsonism: neuropathology. (2012, background): “2009), especially given the fact that fetal mesencephalic intrastriatal transplants to treat PD have been shown to develop Lewy body pathology (Kordower et al. 2008), possibly by cellto-cell transmission (Kordower et al.”
Lysosomal dysfunction increases exosome-mediated alpha-synuclein release and transmission (2011, background): “Host-to-graft propagation of alpha-synuclein-positive Lewylike pathology has recently been demonstrated in long-term mesencephalic transplants in PD patients (Li et al., 2008; Kordower et al. 2008).”
Direct evidence of Parkinson pathology spread from the gastrointestinal tract to the brain in rats (2014, background): “We, and others, have shown that intra-striatal transplants of fetal ventral mesencephalic progenitors in PD patients develop Lewy pathology a decade after transplantation, suggesting transfer of Lewy pathology from the host to the grafted cells [21-23, 29, 30].”
Solution conditions determine the relative importance of nucleation and growth processes in α-synuclein aggregation (2014, background): “Our findings concerning the seeded aggregation of α-synuclein are likely to be of significant physiological importance, not just in the context of the primary growth of fibrils within cells that gives rise to Lewy bodies, but also in the context of the finding that healthy cells can be invaded by α-”
Α-synuclein misfolding and Parkinson's disease. (2012, background): “dopamine transporter over a period of 14 years [89].”
Exogenous α-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells (2009, background): “Also, recent studies indicate that embryonic dopaminergic neurons grafted into PD patients develop -Syn inclusions, suggesting that pathology is conferred by proximity to pathological tissue (26).”
Intracerebral inoculation of pathological α-synuclein initiates a rapidly progressive neurodegenerative α-synucleinopathy in mice (2012, background): “Supporting this hypothesis is the observation that embryonic mesencephalic neurons grafted into the neo striatum of PD patients develop LBs (Kordower et al., 2008; Li et al., 2008).”
Inclusion formation and neuronal cell death through neuron-to-neuron transmission of α-synuclein (2009, background): “However, we also should consider the possibility that the cell death observed in our study is an exaggerated phenotype only present in overexpression-based systems, because no apparent cell death was observed in human transplantation cases (9, 10, 29).”