New advances in brain-targeting nano-drug delivery systems for Alzheimer's disease

Ouyang, Qin; Meng, Yingcai; Zhou, Wenhu; Tong, Jianbin; Cheng, Zhixiang; Zhu, Qubo

doi:10.1080/1061186x.2021.1927055

Cited by 43 publications

(26 citation statements)

References 186 publications

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“…The combined nanoscience and pharmaceutical science application is very promising and has multiplied recently. Therefore, there has been a huge demand for the use of NPs in the last few decades. − Metal-based NPs, such as gold NPs (GNPs), are readily synthesized in various sizes and shapes, easily functionalized, and considered inert and highly stable against oxidation in biological environments and crossing the blood–brain barrier. , GNPs are generally considered to be nontoxic and biocompatible with a high surface-area-to-volume ratio and can be functionalized with a high density of ligands for drug delivery. − …”

Section: Introductionmentioning

confidence: 99%

Inhibition Of Tau Protein Aggregation By a Chaperone-like β-Boswellic Acid Conjugated To Gold Nanoparticles

Gharb

Nouralishahi

Riazi³

et al. 2022

ACS Omega

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A potential therapeutic strategy to inhibit tau protein aggregation in neurons has substantial effects on preventing or controlling Alzheimer’s disease (AD). In this work, we designed a covalent and noncovalent conjugation of β-boswellic acid (BA) to gold nanoparticles (GNPs). We provided the opportunity to investigate the effect of the surface composition of BA-GNPs on the aggregation of the tau protein 1N/4R isoform in vitro. HR-TEM and FESEM micrographs revealed that GNPs were spherical and uniform, smaller than 25 nm. According to UV–visible and FTIR data, BA was successfully conjugated to GNPs. The finding illustrates the effect of the surface charge, size, and hydrophobicity of BA-GNPs on the kinetics of tau protein aggregation. The size and surface area of U-G-BA demonstrated that inhibited tau aggregation more effectively than covalently linked BA. The proposed method for preventing tau aggregation was monomer reduction. At the same time, a chaperone-like feature of GNP-BA while sustaining a tau native structure prevented the additional formation of fibrils. Overall, this study provides insight into the interaction of GNP-BAs with a monomer of tau protein and may suggest novel future therapies for AD.

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Section: Introductionmentioning

confidence: 99%

Inhibition Of Tau Protein Aggregation By a Chaperone-like β-Boswellic Acid Conjugated To Gold Nanoparticles

Gharb

Nouralishahi

Riazi³

et al. 2022

ACS Omega

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“…One such obvious barrier in targeting nutrient transporters is the occurrence of off-target effects due to the abundant expression of nutrient transporters in healthy cells in a variety of tissues [8]. On the other hand, pathological conditions can also lead to changes in the expression pattern of certain transporters [32], for example, GLUT1 expression in the BBB is decreased in patients in an early stage of Alzheimer's disease [30,410]. It should also be taken into account that the application of transporter-targeted formulations may itself also affect the expression level of the corresponding transporter, including depletion from the cell surface [8,26,29,101,111,123,344,360].…”

Section: Discussionmentioning

confidence: 99%

“…A variety of chemical substances have been used as nanocarriers and substrates for further chemical modification to fine-tune pharmacokinetic properties. Among them, liposomes or liposome-based formulations such as functionalized liposomes [8,10,26,29,30], solid lipid nanoparticles/nanostructured lipid carriers [31], various polymer-based nanomicelles/nanoparticles [8,30,[32][33][34][35][36][37][38][39], carbon dots [40], mesoporous silica nanoparticles [41,42] or nanoemulsions [43] have been used for functionalization and transporter-targeted drug delivery.…”

Section: Strategies For Utilizing Transporters For Drug Deliverymentioning

confidence: 99%

Transporter-Mediated Drug Delivery

Gyimesi¹,

Hediger²

2022

Preprint

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Transmembrane transport of small organic and inorganic molecules is one of the cornerstones of cellular metabolism. Among transmembrane transporters, solute carrier (SLC) proteins form the largest, albeit very diverse, superfamily with over 400 members. It has been early on recognized that xenobiotics can directly interact with SLCs and that this interaction can fundamentally determine their efficacy, including bioavailability and intertissue distribution. Apart from the well-established prodrug strategy, the chemical ligation of transporter substrates to nanoparticles of various chemical composition has recently been used as a means to enhance their targeting or absorption. In this review, we summarize efforts in drug design exploiting interactions with specific SLC transporters to optimize their therapeutic effects. Furthermore, we describe current and future challenges as well as new directions for the advanced development of therapeutics that target SLC transporters.

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“…No doubt, as mentioned above, the novel and repurposed drugs are potential candidates to target microglial activation either via the inhibition of M1 microglia activation or via the transition of M1 to M2 macrophages. However, these drugs possess pharmacological as well as pharmacokinetic limitations [80]. The pharmacological limitations can be understood in terms of their systemic side effects on vital organs.…”

Section: Limitations Of Existing Targeted Drugs To Combat Admentioning

confidence: 99%

Mechanisms Involved in Microglial-Interceded Alzheimer’s Disease and Nanocarrier-Based Treatment Approaches

Shadab

Alhakamy

Alfaleh

et al. 2021

JPM

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Alzheimer’s disease (AD) is a common neurodegenerative disorder accountable for dementia and cognitive dysfunction. The etiology of AD is complex and multifactorial in origin. The formation and deposition of amyloid-beta (Aβ), hyperphosphorylated tau protein, neuroinflammation, persistent oxidative stress, and alteration in signaling pathways have been extensively explored among the various etiological hallmarks. However, more recently, the immunogenic regulation of AD has been identified, and macroglial activation is considered a limiting factor in its etiological cascade. Macroglial activation causes neuroinflammation via modulation of the NLRP3/NF-kB/p38 MAPKs pathway and is also involved in tau pathology via modulation of the GSK-3β/p38 MAPK pathways. Additionally, microglial activation contributes to the discrete release of neurotransmitters and an altered neuronal synaptic plasticity. Therefore, activated microglial cells appear to be an emerging target for managing and treating AD. This review article discussed the pathology of microglial activation in AD and the role of various nanocarrier-based anti-Alzeihmenr’s therapeutic approaches that can either reverse or inhibit this activation. Thus, as a targeted drug delivery system, nanocarrier approaches could emerge as a novel means to overcome existing AD therapy limitations.

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New advances in brain-targeting nano-drug delivery systems for Alzheimer's disease

Cited by 43 publications

References 186 publications

Inhibition Of Tau Protein Aggregation By a Chaperone-like β-Boswellic Acid Conjugated To Gold Nanoparticles

Inhibition Of Tau Protein Aggregation By a Chaperone-like β-Boswellic Acid Conjugated To Gold Nanoparticles

Transporter-Mediated Drug Delivery

Mechanisms Involved in Microglial-Interceded Alzheimer’s Disease and Nanocarrier-Based Treatment Approaches

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