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Paula Desplats

Researcher at University of California, San Diego

Publications -  64
Citations -  7536

Paula Desplats is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Neurodegeneration & Alpha-synuclein. The author has an hindex of 33, co-authored 60 publications receiving 6555 citations. Previous affiliations of Paula Desplats include Scripps Research Institute & University of California, Los Angeles.

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Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein.

TL;DR: It is shown that α-synuclein is transmitted via endocytosis to neighboring neurons and neuronal precursor cells, forming Lewy-like inclusions, which provide critical insights into the mechanism of pathological progression in PD and other proteinopathies.
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In vivo demonstration that alpha-synuclein oligomers are toxic.

TL;DR: It is shown that α-syn oligomers are toxic in vivo and thatα- syn variants that form oligomers might interact with and potentially disrupt membranes and the toxicity of these mutants by using a rat lentivirus system to investigate loss of dopaminergic neurons in the substantia nigra.
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Selective Molecular Alterations in the Autophagy Pathway in Patients with Lewy Body Disease and in Models of α-Synucleinopathy

TL;DR: This study supports the notion that defects in the autophagy pathway and more specifically in mTor and Atg7 are associated with neurodegeneration in DLB cases and α-synuclein transgenic models and supports the possibility that modulators of the autophile pathway might have potential therapeutic effects.
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Antibody-Aided Clearance of Extracellular α-Synuclein Prevents Cell-to-Cell Aggregate Transmission

TL;DR: It is shown that antibodies against α- synuclein specifically target and aid in clearance of extracellular α-synuclein proteins by microglia, thereby preventing their actions on neighboring cells.
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The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice

TL;DR: Chronic oral administration of HDACi 4b, beginning after the onset of motor deficits, significantly improved motor performance, overall appearance, and body weight of symptomatic R6/2300Q transgenic mice, and may offer clinical benefit for HD patients and provide a novel set of potential biomarkers for clinical assessment.