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Maeve A. Caldwell

Researcher at Trinity College, Dublin

Publications -  86
Citations -  6180

Maeve A. Caldwell is an academic researcher from Trinity College, Dublin. The author has contributed to research in topics: Neural stem cell & Stem cell. The author has an hindex of 39, co-authored 83 publications receiving 5820 citations. Previous affiliations of Maeve A. Caldwell include University of Cambridge & École Polytechnique Fédérale de Lausanne.

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A new method for the rapid and long term growth of human neural precursor cells

TL;DR: This simple and novel culture method allows the rapid expansion of large numbers of non-transformed human neural precursor cells which may be of use in drug discovery, ex vivo gene therapy and clinical neural transplantation.
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Long-Term Survival of Human Central Nervous System Progenitor Cells Transplanted into a Rat Model of Parkinson's Disease ☆

TL;DR: Results show that expanded populations of human CNS progenitor cells maintained in a proliferative state in culture can migrate and differentiate into both neurons and astrocytes following intracerebral grafting, and may have potential for development as an alternative source of tissue for neural transplantation in degenerative diseases.
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Growth factors regulate the survival and fate of cells derived from human neurospheres

TL;DR: It is shown that maintaining cell–cell contact during the differentiation stage, in combination with growth factor administration, can increase the number of neurons generated under serum-free conditions from 8% to >60%.
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Human neural precursor cells express low levels of telomerase in vitro and show diminishing cell proliferation with extensive axonal outgrowth following transplantation

TL;DR: It is shown that human neural precursor cells express very low levels of telomerase at early passages, but that this decreases to undetectable levels at later passages, which may provide the ideal basis for the repair of other lesions of the CNS where extensive axonal outgrowth is required.
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Parkinson's disease–associated mutant VPS35 causes mitochondrial dysfunction by recycling DLP1 complexes

TL;DR: It is demonstrated that PD-associated VPS35 mutations caused mitochondrial fragmentation and cell death in cultured neurons in vitro, in mouse substantia nigra neurons in vivo and in human fibroblasts from an individual with PD who has the VPS 35D620N mutation.