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Dorit Farfara
Researcher at Tel Aviv University
Publications - 20
Citations - 1147
Dorit Farfara is an academic researcher from Tel Aviv University. The author has contributed to research in topics: Innate immune system & Alzheimer's disease. The author has an hindex of 11, co-authored 18 publications receiving 1015 citations. Previous affiliations of Dorit Farfara include University of California, San Diego & Rockefeller University.
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Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer's disease
TL;DR: The immune response in the AD brain is regulated by Glial cells, which mediate the peripheral immune response and activation as a therapeutic target in AD is studied.
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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
Limor Avrahami,Dorit Farfara,Maya Shaham-Kol,Robert Vassar,Dan Frenkel,Hagit Eldar-Finkelman +5 more
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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Orally administrated cinnamon extract reduces β-amyloid oligomerization and corrects cognitive impairment in Alzheimer's disease animal models.
Anat Frydman-Marom,Aviad Levin,Dorit Farfara,Tali Benromano,Roni Scherzer-Attali,Sivan Peled,Robert Vassar,Daniel L. Segal,Ehud Gazit,Dan Frenkel,Michael Ovadia +10 more
TL;DR: A novel prophylactic approach for inhibition of toxic oligomeric Aβ species formation in AD is presented through the utilization of a compound that is currently in use in human diet, based on cinnamon extract, which markedly inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ on neuronal PC12 cells.
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Scara1 deficiency impairs clearance of soluble amyloid-β by mononuclear phagocytes and accelerates Alzheimer's-like disease progression.
Dan Frenkel,Kim Wilkinson,Lingzhi Zhao,Suzanne E. Hickman,Terry K. Means,Lindsay Puckett,Dorit Farfara,Nathan D. Kingery,Howard L. Weiner,Joseph El Khoury +9 more
TL;DR: Scara1 deficiency markedly accelerates Aβ accumulation leading to increased mortality, and pharmacological upregulation of Scara1 expression on mononuclear phagocytes increases Aβ clearance, which is a potential treatment strategy for Alzheimer’s disease.
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Toll-Like Receptors Expression and Signaling in Glia Cells in Neuro-Amyloidogenic Diseases: Towards Future Therapeutic Application
TL;DR: Understanding the pattern of TLR signaling in glial cells in neurodegenerative diseases such as Alzheimer's disease, prion diseases, amyotrophic lateral sclerosis, and Parkinson's disease may lead to the identification of new targets for therapeutic application.