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Efrat Levy

Researcher at Nathan Kline Institute for Psychiatric Research

Publications -  23
Citations -  729

Efrat Levy is an academic researcher from Nathan Kline Institute for Psychiatric Research. The author has contributed to research in topics: Exosome & Cystatin C. The author has an hindex of 12, co-authored 23 publications receiving 462 citations.

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Mitovesicles are a novel population of extracellular vesicles of mitochondrial origin altered in Down syndrome.

TL;DR: Using a high-resolution density gradient separation of extracellular vesicles (EVs) isolated from murine and human DS and diploid control brains, this paper identified and characterized a previously unknown population of double-membraned EVs containing multiple mitochondrial proteins distinct from previously described EV subtypes, including microvesicles and exosomes.
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Enhanced exosome secretion in Down syndrome brain - a protective mechanism to alleviate neuronal endosomal abnormalities

TL;DR: It is found that exosome secretion is enhanced in the brains of DS patients and a mouse model of the disease, and by DS fibroblasts, and increased levels of the tetraspanin CD63, a regulator ofExosome biogenesis, were observed in DS brains, suggesting the upregulation of exosomes represents a potential therapeutic goal for neurodegenerative disorders with endosomal pathology.
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The Endosomal-Lysosomal Pathway Is Dysregulated by APOE4 Expression in Vivo.

TL;DR: Findings directly link the APOE4 genotype to endosomal–lysosomal dysregulation in an in vivo, AD pathology-free setting, which may play a causative role in the increased incidence of AD among APoe4 carriers.
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Apolipoprotein E4 genotype compromises brain exosome production.

TL;DR: Using human and mouse tissue, Peng et al. report that APOE4 reduces brain exosome production and release, which may be the initial event in endosomal-lysosome-exosomal alterations contributing to neuronal vulnerability and neurodegenerative risk in APoe4-carriers.
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Age-dependent dysregulation of brain amyloid precursor protein in the Ts65Dn Down syndrome mouse model.

TL;DR: Brain levels of both Aβ40 and Aβ42 were not increased in Ts65Dn mice compared with diploid mice at all ages examined, suggesting multiple mechanisms contribute to the regulation towards diploids levels of APP metabolites in the Ts 65Dn mouse brain.