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Dan Frenkel

Researcher at Tel Aviv University

Publications -  12
Citations -  715

Dan Frenkel is an academic researcher from Tel Aviv University. The author has contributed to research in topics: P3 peptide & Biochemistry of Alzheimer's disease. The author has an hindex of 10, co-authored 12 publications receiving 605 citations.

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Phenylalanine assembly into toxic fibrils suggests amyloid etiology in phenylketonuria.

TL;DR: It is demonstrated that at pathological concentrations, phenylalanine self-assembles into fibrils with amyloid-like morphology and well-ordered electron diffraction, suggesting a new amyloidsosis-like etiology for PKU.
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Inhibition of Glycogen Synthase Kinase-3 Ameliorates β-Amyloid Pathology and Restores Lysosomal Acidification and Mammalian Target of Rapamycin Activity in the Alzheimer Disease Mouse Model IN VIVO AND IN VITRO STUDIES

TL;DR: Inhibition of GSK-3 restores lysosomal acidification that in turn enables clearance of Aβ burdens and reactivation of mTOR, which facilitates amelioration in cognitive function and provides evidence that mTOR is a target activated by G SKS-3 but inhibited by impaired lysOSomal Acidification and elevation in amyloid precursor protein/Aβ loads.
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Characterization of brain lesions in a mouse model of progressive multiple sclerosis

TL;DR: It is shown that immunization of non-obese diabetic (NOD) mice with myelin oligodendrocyte glycoprotein peptide 35-55 leads to the development of relapsing-remitting stages, evident from days 20 to 70, which then develops into a chronic progressive stage, similar to MS stages found in humans.
Patent

Filamentous bacteriophage displaying an β-amyloid epitope

TL;DR: In this article, a strategy for immunizing against amyloid plaques using display technology is presented, which includes methods, agents, and pharmaceutical compositions for vaccination against plaque forming diseases (e.g. Alzheimer's disease) which rely upon presentation of an antigen or epitope on a display vehicle.
Journal ArticleDOI

Expression of Scavenger receptor A on antigen presenting cells is important for CD4+ T-cells proliferation in EAE mouse model

TL;DR: Immunological assessment showed that SRA deficiency resulted in significant reduction of pro-inflammatory cytokines that play a major role in EAE progression, such as IL-2, IFN-gamma, IL-17 and IL-6, and SRA−/− APCs showed impairments in activation and in their ability to induce pro- inflammatory CD4+ T cell proliferation.