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Biomimetic Nanocarrier Targeting Drug(s) to Upstream-Receptor Mechanisms in Dementia: Focusing on Linking Pathogenic Cascades

Cavitation-Control Technology Inc., Farmington, CT 06032, USA
Present address: Cav-Con Inc., Bellevue, WA 98007, USA.
Biomimetics 2020, 5(1), 11; https://doi.org/10.3390/biomimetics5010011
Received: 21 January 2020 / Revised: 14 March 2020 / Accepted: 19 March 2020 / Published: 20 March 2020
Past published studies have already documented that, subsequent to the intravenous injection of colloidal lipid nanocarriers, apolipoprotein (apo)A-I is adsorbed from the blood onto the nanoparticle surface. The adsorbed apoA-I mediates the interaction of the nanoparticle with scavenger receptors on the blood–brain barrier (BBB), followed by receptor-mediated endocytosis and subsequent transcytosis across the BBB. By incorporating the appropriate drug(s) into biomimetic (lipid cubic phase) nanocarriers, one obtains a multitasking combination therapeutic which targets certain cell-surface scavenger receptors, mainly class B type I (i.e., SR-BI), and crosses the BBB. Documented similarities in lipid composition between naturally occurring high-density lipoproteins (HDL) and the artificial biomimetic (nanoemulsion) nanocarrier particles can partially simulate or mimic the known heterogeneity (i.e., subpopulations or subspecies) of HDL particles. Such biomedical application of colloidal drug-nanocarriers can potentially be extended to the treatment of complex medical disorders like dementia. The risk factors for dementia trigger widespread inflammation and oxidative stress; these two processes involve pathophysiological cascades which lead to neuronal Ca2+ increase, neurodegeneration, gradual cognitive/memory decline, and eventually (late-onset) dementia. In particular, more recent research indicates that chronic inflammatory stimulus in the gut may induce (e.g., via serum amyloid A (SAA)) the release of proinflammatory cytokines. Hence, an effective preventive and therapeutic strategy could be based upon drug targeting toward a major SAA receptor responsible for the SAA-mediated cell signaling events leading to cognitive decline and eventually Alzheimer’s disease or (late-onset) dementia. View Full-Text
Keywords: Alzheimer’s disease; calcium dyshomeostasis; dementia; drug targeting; endothelial dysfunction; inflammation; nanocarrier; oxidative stress Alzheimer’s disease; calcium dyshomeostasis; dementia; drug targeting; endothelial dysfunction; inflammation; nanocarrier; oxidative stress
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D’Arrigo, J.S. Biomimetic Nanocarrier Targeting Drug(s) to Upstream-Receptor Mechanisms in Dementia: Focusing on Linking Pathogenic Cascades. Biomimetics 2020, 5, 11.

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