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Juliana Bender Hoppe

Researcher at Universidade Federal do Rio Grande do Sul

Publications -  38
Citations -  1406

Juliana Bender Hoppe is an academic researcher from Universidade Federal do Rio Grande do Sul. The author has contributed to research in topics: Neuroprotection & Neuroinflammation. The author has an hindex of 20, co-authored 36 publications receiving 1165 citations. Previous affiliations of Juliana Bender Hoppe include University of Reading.

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Free and nanoencapsulated curcumin suppress β-amyloid-induced cognitive impairments in rats: Involvement of BDNF and Akt/GSK-3β signaling pathway

TL;DR: The findings demonstrate that administration of curcumin was effective in preventing behavioral impairments, neuroinflammation, tau hyperphosphorylation as well as cell signaling disturbances triggered by Aβ in vivo, and suggest thatCur-LNC in a dose 20-fold lower presented similar neuroprotective results compared to the effective dose of free curcuming.
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Characterization of trans-resveratrol-loaded lipid-core nanocapsules and tissue distribution studies in rats.

TL;DR: Trans-Resveratrol-loaded lipid-core nanocapsules increased the concentration of trans-resver atrol in the brain tissue and Gastrointestinal safety was improved and may be used as an alternative potential therapeutic for several diseases including Alzheimer's disease.
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Neuroprotective Effects of Resveratrol Against Aβ Administration in Rats are Improved by Lipid-Core Nanocapsules

TL;DR: The results clearly show that by using lipid-core nanocapsules, resveratrol was able to rescue the deleterious effects of Aβ1-42 while treatment with RSV presented only partial beneficial effects.
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A Comparative Study of β-Amyloid Peptides Aβ1-42 and Aβ25-35 Toxicity in Organotypic Hippocampal Slice Cultures

TL;DR: Comparing two commonly used Aβ peptides on an in-vitro model of Aβ toxicity provides strong evidence that Aβ1-42 and the Aβ25-35 peptides induce neural injury in a similar pattern and that A β25- 35 is a convenient tool for the investigation of neurotoxic mechanisms involved in AD.
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Amyloid‐β neurotoxicity in organotypic culture is attenuated by melatonin: involvement of GSK‐3β, tau and neuroinflammation

TL;DR: It is speculated that melatonin may provide an effective therapeutic strategy for AD, by attenuating Aβ‐induced phosphorylation of tau protein, and preventing GSK‐3β activation and neuroinflammation.