Emanuela Cazzaniga

TL;DR: Bi-functionalized liposomes with phosphatidic acid and a modified ApoE-derived peptide were demonstrated to influence Aβ aggregation/disaggregation as a potential treatment in an Alzheimer's model and were able to cross the blood-brain barrier in vitro and in vivo.

TL;DR: It is suggested for the first time that an early Pin1 response might be transiently evoked by Abeta 1-42 oligomers, preventing Tau hyperphosphorylation, highlighting the role of Pin1 as Tau phosphorylation modulator during Alzheimer onset.

TL;DR: It is pointed out that ischemic events may directly contribute in brain capillary endothelial cells to the enhancement of the amyloidogenic metabolism, leading to intracellular deposition of Aβ(42), which may contribute to the impairment of A β brain clearance and AD related blood brain barrier dysfunctions.

TL;DR: The results suggest that MSNPs may be low-risk if prepared with a diameter <30 nm and if they reach human tissues at doses <0.25 mg/mL, and could help the rational design of NPs intended for biomedical uses, demonstrating that careful toxicity evaluation is necessary before using MSnPs in patients.

TL;DR: The data suggested that Au@PMA reduced the cell viability mostly through oxidative stress and TNF-α production after the uptake by HUVECs and macrophages, respectively.