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Ole Isacson

Researcher at Harvard University

Publications -  349
Citations -  31997

Ole Isacson is an academic researcher from Harvard University. The author has contributed to research in topics: Transplantation & Dopaminergic. The author has an hindex of 93, co-authored 345 publications receiving 30460 citations. Previous affiliations of Ole Isacson include Hanyang University & Istituto Italiano di Tecnologia.

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Parkinson’s Disease Patient-Derived Induced Pluripotent Stem Cells Free of Viral Reprogramming Factors

TL;DR: In this paper, the authors showed that fibroblasts from five patients with idiopathic Parkinson's disease can be efficiently reprogrammed and subsequently differentiated into dopaminergic neurons using Cre-recombinase excisable viruses.
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Neurons derived from reprogrammed fibroblasts functionally integrate into the fetal brain and improve symptoms of rats with Parkinson's disease

TL;DR: It is shown that iPS cells can be efficiently differentiated into neural precursor cells, giving rise to neuronal and glial cell types in culture and demonstrating the therapeutic potential of directly reprogrammed fibroblasts for neuronal cell replacement in the animal model.
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Embryonic stem cells develop into functional dopaminergic neurons after transplantation in a Parkinson rat model

TL;DR: It is shown that transplanting low doses of undifferentiated mouse embryonic stem cells into the rat striatum results in a proliferation of ES cells into fully differentiated DA neurons that can restore cerebral function and behavior in an animal model of Parkinson's disease.
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Specific MicroRNAs Modulate Embryonic Stem Cell–Derived Neurogenesis

TL;DR: It is concluded that distinct miRNAs play a functional role in the determination of neural fates in ES cell differentiation, and evidence that signal transducer and activator of transcription (STAT) 3, a member of the STAT family pathway, is involved in the function of these mi RNAs is provided.
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Altered Proteasomal Function in Sporadic Parkinson's Disease

TL;DR: It is suggested that failure of the ubiquitin-proteasome system to adequately clear unwanted proteins may underlie vulnerability and degeneration of the SNc in both sporadic and familial PD.