Titanium dioxide and carbon black nanoparticles disrupt neuronal homeostasis via excessive activation of cellular prion protein signaling

ABD

Industry: Biopharmaceutics
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Instrument: Vasco Kin

Industry: Biopharmaceutics

DOI: https://doi.org/10.1186/s12989-022-00490-x

Keywords: Nanoparticles, PrPC receptor, Signaling, TNFα receptors, Aβ peptides, Neuroinfammation, Nanoneurotoxicity, Alzheimer’s disease

Epidemiological emerging evidence shows that human exposure to some nanosized materials present in the environment would contribute to the onset and/or progression of Alzheimer’s disease (AD). The cellular and molecular mechanisms whereby nanoparticles would exert some adverse effects towards neurons and take part in AD pathology are nevertheless unknown. (319)

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