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Table 4 Selected relevant pre-clinical studies based on recent PNPs for the diagnosis and treatment of AD

From: Nanomedicine-based technologies and novel biomarkers for the diagnosis and treatment of Alzheimer’s disease: from current to future challenges

Loaded molecule Polymeric matrix Surface modifications Dose Admin. route In vitro/in vivo model Results Refs
Lutein PLGA Chitosan 0–20 mM Incubation SHSY-5Y cells
RPMI 2650 cells
NPs are highly deposited in brain following i.n. route and demonstrated to possess significant ROS scavenging activity Dhas et al. [174]
4 mg LT/kg i.n Sprague Dawley rats
10 μM Incubation bEnd.3 cells
PC12 cells
HT22 cells
CTX-TNA2 cells
TPL-PNPs show higher binding affinity to either GT1b ganglioside receptor or brain capillary endothelial bEnd.3 cells, increase the BBB-penetration and neuron-targeting efficacy, enhance ROS scavenging ability and protect microtubule from Aβ25‐35-induced neurotoxicity, inhibit okadaic acid-induced tau aggregation and neuronal apoptosis, improve the cognitive performance of treated mice, down-regulate the tau phosphorylation level, promote axonal transport and attenuate microgliosis Guo et al. [185]
6–24 μg NPs/kg/day N.A ICR mice
Chitosan Eu(NO3)3
0.67 mg/ml NPs-CSF sample
AD rats Developed NPs act as a ratiometric fluorescent probe for the detection of Aβ monomers. In CSF and various brain tissues of rats, developed NPs are able to recognize the Aβ peptide and fluoresce, thus leading to its detection and quantification Liu et al. [181]
Phytol PLGA 5–10 µg/ml Incubation Neuro-2a cells PNPs increase the lifespan, chemotaxis behaviour and decrease Aβ deposition and ROS production in the in vivo models of AD. Moreover, PNPs treatment downregulate the expression of AD associated genes viz Aβ, ace-1 and hsp-4 upregulate the gene dnj-14, involved in the longevity of nematodes, and reduce the expression of Aβ peptide at the protein level Sathya et al. [176]
25, 50 and 100 μg/ml Exposition Caenorhabditis elegans (CL2006, CL4176)
Curcumin PLGA [Gd]DTPA
100 µCi/100 µL i.v Tg2576 mice NPs improve BBB transcytosis by coating with a K16ApoE
NPs enhance MRI contrast to detect Aβ plaques
Ahlschwede et al. [180]
EGCG/AA PLGA PEG 15–500 μg/ml Incubation BMVECs NPs effectively penetrate through the in vitro BBB without damaging the BBB integrity. NPs treatment reduce neuroinflammation, Aβ plaque burden, soluble and insoluble Aβ42 peptide levels
and enhance synapsis expression, spatial learning and memory processes
Cano et al. [178]
40 mg/kg/day v.o APP/PS1 mice
DBP PLGA 2.5 mg/kg i.v 5XFAD mice Inhibition Aβ aggregation in vitro. Attenuation of Aβ accumulation, neuroinflammation, neuronal loss and cognitive dysfunction Jeon et al. [182]
  1. AA, ascorbic acid; BMVECs, brain microvascular endothelial cells; CDs, carbon dots; CSF, cerebrospinal fluid; DBP, Vitamin D-binding protein; EGCG; Epigallocatechin-3-gallate; GMP, guanosine monophosphate disodium; NAP, neuroprotective peptide; ROS, Reactive oxygen species; TPL, fusion peptide comprising a BBB-penetrating peptide TGN and a neuron binding peptide Tet1