Advanced fabrication approaches to controlled delivery systems for epilepsy treatment

Tienderen, Gilles Sebastiaan van; Berthel, Marius; Yue, Zhilian; Cook, Mark; Liu, Xiao; Beirne, Stephen; Wallace, Gordon G.

doi:10.1080/17425247.2018.1517745

Cited by 17 publications

(16 citation statements)

References 81 publications

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“…In general, drug delivery from GelMA is mediated by diffusion and degradation. 16 At first, diffusion dominances the release profile because matrix degradation is slow. 17 Drug is immobilized by macro/nano-entrapment.…”

Section: Discussionmentioning

confidence: 99%

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Controlled Release of Naringin in GelMA-Incorporated Rutile Nanorod Films to Regulate Osteogenic Differentiation of Mesenchymal Stem Cells

et al. 2019

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Naringin, a Chinese herbal medicine, has been demonstrated to concentration-dependently promote osteogenic differentiation of mesenchymal stem cells (MSCs). However, it remains a challenge to load naringin on coatings for osteogenesis and further control the release kinetics. Here, we demonstrated that the release behavior of naringin on rutile nanorod films could be controlled by either mixing naringin with gelatin methacryloyl (GelMA) before spinning onto the films or soaking the obtained GelMA-incorporated films with the naringin solution to achieve the distinct degradation-type release and diffusion-type release, respectively. We further revealed that the naringin-loaded coatings facilitated adhesion, proliferation and late differentiation, and mineralization of MSCs. Our findings provided a novel strategy to engineer the coatings with controlled release of naringin and emphasized the bioactivity of naringin for the osteogenic differentiation of MSCs.

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Section: Discussionmentioning

confidence: 99%

“…18−20 The degradation of GelMA can be divided into bulk and surface erosion. 16 Bulk erosion is homogenous when GelMA swelling is faster than the polymer disintegration. In contrast, surface erosion is heterogeneous when the polymer disintegration is predominant.…”

Section: Discussionmentioning

confidence: 99%

Controlled Release of Naringin in GelMA-Incorporated Rutile Nanorod Films to Regulate Osteogenic Differentiation of Mesenchymal Stem Cells

et al. 2019

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“…As described above, BBB alterations in the epileptic brain may restrict brain entry of several major ASDs, which may add to the problem of drug resistance in epilepsy. There are various invasive and non-invasive strategies to bypass the BBB [110]; among those, local drug delivery is the strategy that has been most widely explored in epilepsy research [111][112][113][114]. ASDs or other neuroactive compounds may be either directly injected into the epileptic focus, for example, the hippocampus, or into the cerebrospinal fluid (CSF) by intracerebroventricular (i.c.v.)…”

Section: Overcoming the Bbb In Epilepsy By Delivering Therapeutics Tomentioning

confidence: 99%

Structural, Molecular, and Functional Alterations of the Blood-Brain Barrier during Epileptogenesis and Epilepsy: A Cause, Consequence, or Both?

Löscher¹,

Friedman

2020

IJMS

165

117

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The blood-brain barrier (BBB) is a dynamic, highly selective barrier primarily formed by endothelial cells connected by tight junctions that separate the circulating blood from the brain extracellular fluid. The endothelial cells lining the brain microvessels are under the inductive influence of neighboring cell types, including astrocytes and pericytes. In addition to the anatomical characteristics of the BBB, various specific transport systems, enzymes and receptors regulate molecular and cellular traffic across the BBB. While the intact BBB prevents many macromolecules and immune cells from entering the brain, following epileptogenic brain insults the BBB changes its properties. Among BBB alterations, albumin extravasation and diapedesis of leucocytes from blood into brain parenchyma occur, inducing or contributing to epileptogenesis. Furthermore, seizures themselves may modulate BBB functions, permitting albumin extravasation, leading to activation of astrocytes and the innate immune system, and eventually modifications of neuronal networks. BBB alterations following seizures are not necessarily associated with enhanced drug penetration into the brain. Increased expression of multidrug efflux transporters such as P-glycoprotein likely act as a ‘second line defense’ mechanism to protect the brain from toxins. A better understanding of the complex alterations in BBB structure and function following seizures and in epilepsy may lead to novel therapeutic interventions allowing the prevention and treatment of epilepsy as well as other detrimental neuro-psychiatric sequelae of brain injury.

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“…Different technical strategies aim to achieve network-specific pharmacological seizure-control in contrast to systemic drug treatment. Concerning direct intracranial drug delivery, several techniques ( Figure 3) to administer drugs locally to the brain are investigated and discussed in detail in numerous excellent reviews, e.g., [13,[43][44][45][46][47][48][49][50][51][52]. Overview of application routes for intracranial drug delivery in epilepsies resistant to systemically administered antiseizure drugs.…”

Section: Technical Considerationsmentioning

confidence: 99%

“…An approach to prolong the duration of antiseizure effects by intracranial drug delivery is the use of drug-loaded biodegradable or nonbiodegradable polymer-based implants or bioceramics slowly releasing ASDs or other appropriate compounds, which then passively diffuse through the surrounding tissue. These drug carriers are experimentally implanted at seizure-modulating brain targets in order to achieve a gradual, more or less continuous drug release directly into the target region of the epileptic network [43,44]. Although the capacity of such carriers is limited, controlled-release polymers have reproducible release kinetics capable of releasing drugs over a period of days to years.…”

Section: Technical Considerationsmentioning

confidence: 99%

Bypassing the Blood–Brain Barrier: Direct Intracranial Drug Delivery in Epilepsies

Gernert¹,

Feja²

2020

Pharmaceutics

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Epilepsies are common chronic neurological diseases characterized by recurrent unprovoked seizures of central origin. The mainstay of treatment involves symptomatic suppression of seizures with systemically applied antiseizure drugs (ASDs). Systemic pharmacotherapies for epilepsies are facing two main challenges. First, adverse effects from (often life-long) systemic drug treatment are common, and second, about one-third of patients with epilepsy have seizures refractory to systemic pharmacotherapy. Especially the drug resistance in epilepsies remains an unmet clinical need despite the recent introduction of new ASDs. Apart from other hypotheses, epilepsy-induced alterations of the blood–brain barrier (BBB) are thought to prevent ASDs from entering the brain parenchyma in necessary amounts, thereby being involved in causing drug-resistant epilepsy. Although an invasive procedure, bypassing the BBB by targeted intracranial drug delivery is an attractive approach to circumvent BBB-associated drug resistance mechanisms and to lower the risk of systemic and neurologic adverse effects. Additionally, it offers the possibility of reaching higher local drug concentrations in appropriate target regions while minimizing them in other brain or peripheral areas, as well as using otherwise toxic drugs not suitable for systemic administration. In our review, we give an overview of experimental and clinical studies conducted on direct intracranial drug delivery in epilepsies. We also discuss challenges associated with intracranial pharmacotherapy for epilepsies.

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Advanced fabrication approaches to controlled delivery systems for epilepsy treatment

Cited by 17 publications

References 81 publications

Controlled Release of Naringin in GelMA-Incorporated Rutile Nanorod Films to Regulate Osteogenic Differentiation of Mesenchymal Stem Cells

Controlled Release of Naringin in GelMA-Incorporated Rutile Nanorod Films to Regulate Osteogenic Differentiation of Mesenchymal Stem Cells

Structural, Molecular, and Functional Alterations of the Blood-Brain Barrier during Epileptogenesis and Epilepsy: A Cause, Consequence, or Both?

Bypassing the Blood–Brain Barrier: Direct Intracranial Drug Delivery in Epilepsies

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