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Genevieve Gowing

Researcher at Cedars-Sinai Medical Center

Publications -  37
Citations -  4311

Genevieve Gowing is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Motor neuron. The author has an hindex of 24, co-authored 36 publications receiving 3929 citations. Previous affiliations of Genevieve Gowing include Laval University & University of Wisconsin-Madison.

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Bone Marrow-Derived Microglia Play a Critical Role in Restricting Senile Plaque Formation in Alzheimer's Disease

TL;DR: This work shows a massive infiltration of highly ramified and elongated microglia within the core of amyloid plaques in transgenic mouse models of Alzheimer's disease (AD), and shows that blood-derivedmicroglia and not their resident counterparts have the ability to eliminate amyloids deposits by a cell-specific phagocytic mechanism.
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Selective ablation of proliferating microglial cells exacerbates ischemic injury in the brain.

TL;DR: In vivo evidence of a neuroprotective role of proliferating microglia serving as an endogenous pool of neurotrophic molecules such as IGF-1 is reported, which may open new therapeutic avenues in the treatment of stroke and other neurological disorders.
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Exacerbation of Motor Neuron Disease by Chronic Stimulation of Innate Immunity in a Mouse Model of Amyotrophic Lateral Sclerosis

TL;DR: The effects of acute and chronic administration of lipopolysaccharide (LPS) are addressed in a genetic model of neurodegeneration to provide solid evidence that environmental factors and innate immunity can cooperate to influence the course of disease of an inherited neuropathology.
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Requirement of myeloid cells for axon regeneration.

TL;DR: Myeloid cells support axonal regeneration and functional recovery by creating a growth-permissive milieu for injured axons in the absence of CD11b-TKmt-30 mice.
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A Frameshift Deletion in Peripherin Gene Associated with Amyotrophic Lateral Sclerosis

TL;DR: The results suggest that PRPH mutations may be responsible for a small percentage of ALS, cases and they provide further support of the view that neurofilament disorganization may contribute to pathogenesis.