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Penelope J. Hallett

Researcher at Harvard University

Publications -  55
Citations -  4328

Penelope J. Hallett is an academic researcher from Harvard University. The author has contributed to research in topics: Substantia nigra & Parkinson's disease. The author has an hindex of 32, co-authored 51 publications receiving 3660 citations. Previous affiliations of Penelope J. Hallett include Istituto Italiano di Tecnologia.

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Differentiated Parkinson patient-derived induced pluripotent stem cells grow in the adult rodent brain and reduce motor asymmetry in Parkinsonian rats

TL;DR: The transplantation of human PDiPS cell-derived neurons as a long-term in vivo method to analyze potential disease-related changes in a physiological context is established and proof of principle of survival and functional effects is demonstrated.
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Dopamine neurons implanted into people with Parkinson’s disease survive without pathology for 14 years

TL;DR: Postmortem analysis of five subjects with Parkinson's disease 9–14 years after transplantation of fetal midbrain cell suspensions revealed surviving grafts that included dopamine and serotonin neurons without pathology.
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Successful function of autologous iPSC-derived dopamine neurons following transplantation in a non-human primate model of Parkinson's disease.

TL;DR: The finding that unilateral engraftment of CM-iPSCs could provide a gradual onset of functional motor improvement contralateral to the side of dopamine neuron transplantation, and increased motor activity, without a need for immunosuppression supports further development of autologous iPSC-derived cell transplantation for treatment of PD.
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Rationale for and use of NMDA receptor antagonists in Parkinson's disease.

TL;DR: In animal models, NMDA receptor antagonists are effective antiparkinsonian agents and can reduce the complications of chronic dopaminergic therapy (wearing off and dyskinesias).
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Dopamine D1 Activation Potentiates Striatal NMDA Receptors by Tyrosine Phosphorylation-Dependent Subunit Trafficking

TL;DR: Modification of these pathways may be a useful therapeutic target for Parkinson’s disease and other basal ganglia disorders in which abnormal function of striatal NMDA receptors contributes to the symptoms of the diseases.