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Lisa J. Fisher

Researcher at University of California, San Diego

Publications -  39
Citations -  4818

Lisa J. Fisher is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Transplantation & Substantia nigra. The author has an hindex of 25, co-authored 39 publications receiving 4767 citations. Previous affiliations of Lisa J. Fisher include University of California, Berkeley & Salk Institute for Biological Studies.

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Survival and differentiation of adult neuronal progenitor cells transplanted to the adult brain.

TL;DR: It is indicated that FGF-2 responsive progenitors can be isolated from the adult hippocampus and that these cells retain the capacity to generate mature neurons when grafted into the adult rat brain.
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Isolation, Characterization, and use of Stem Cells from the CNS

TL;DR: Because in vitro culture conditions are unlikely to provide all of the factors necessary for inducing the proliferation and differentiation of neural precursors, recent studies have explored the properties of well-characterized precursor populations after implantation back into specific regions of the developing or adult CNS.
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Essential role of neocortical acetylcholine in spatial memory

TL;DR: This work describes how it achieved a permanent and selective impairment of learning and memory by damaging the nucleus basalis magno-cellularis, a nucleus that provides the major cholinergic innervation of the neocortex in adult rats, and test the hypothesis that acetylcholine is essential for restoration of cognitive function.
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Grafting fibroblasts genetically modified to produce L-dopa in a rat model of Parkinson disease.

TL;DR: Only grafts containing TH-expressing fibroblasts were found to reduce rotational asymmetry and have general implications for the application of gene therapy to human neurological disease and specific implications for Parkinson disease.
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Survival and function of intrastriatally grafted primary fibroblasts genetically modified to produce L-dopa.

TL;DR: It is suggested that primary fibroblasts genetically altered to express TH have the capacity to deliver L-dopa locally to the striatum in quantities sufficient to compensate partially for the loss of intrinsic striatal dopaminergic input.