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Unveiling Molecular Mysteries of Brain Barriers
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Unveiling Molecular Mysteries of Brain Barriers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 1297

Special Issue Editor

Dr. Ana Catarina Duarte

E-Mail Website
Guest Editor
1. CICS-UBI, Health Sciences Research Centre, University of Beira Interior, Covilhã, Portugal
2. UDI-IPG- Unidade de Investigação para o Desenvolvimento do Interior, Instituto Politécnico da Guarda, Guarda, Portugal
Interests: brain barriers; choroid plexus; chemical surveillance; taste signaling

Special Issue Information

Dear Colleagues,

The brain is protected by specialized barriers, including the blood–brain barrier (BBB), blood–cerebrospinal fluid barrier (BCSFB), and the arachnoid barrier (AB). These barriers rely on tightly regulated molecular mechanisms. Tight junction proteins seal endothelial cells at the BBB and epithelial choroid plexus cells at the BCSFB, limiting paracellular transport. Active efflux systems, such as ATP-binding cassette (ABC) transporters, regulate molecular exchange, preventing neurotoxic accumulation while maintaining nutrient delivery.

Despite their critical role in brain homeostasis, brain barriers restrict the entry of many therapeutic drugs, posing a challenge for brain drug delivery. Meanwhile, certain peripheral cancers can bypass these barriers to metastasize to the brain. This underscores the need for a deeper understanding of the molecular mechanisms governing brain barriers, particularly those that regulate exchanges between the brain and the periphery.

This Special Issue on “Unveiling Molecular Mysteries of Brain Barriers” aims to explore novel molecular mechanisms and advance therapeutic strategies capable of crossing brain barriers to effectively target brain cells.

Original papers, review articles, and perspectives from experts in the field are welcome.

Dr. Ana Catarina Duarte
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • blood–brain barrier
  • blood–cerebrospinal fluid barrier
  • arachnoid barrier
  • transport mechanisms
  • drug delivery
  • drug metabolism
  • ATP-binding cassete (ABC) transporters

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Published Papers (2 papers)

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18 pages, 1543 KB  
Article
Insulin and Incretin Receptor Agonists Reciprocally Alter Their Blood–Brain Barrier Permeabilities
by Angeline Fry, Alexis Rose, Riley Weaver, Kim Hansen, James E. Blevins, William A. Banks and Elizabeth M. Rhea
Int. J. Mol. Sci. 2026, 27(10), 4611; https://doi.org/10.3390/ijms27104611 - 21 May 2026
Viewed by 189
Abstract
Incretin receptor agonists (IRAs) such as GLP-1-based therapies improve metabolic and cognitive outcomes and enhance brain insulin signaling. One way that IRAs could have these actions is by affecting the blood–brain barrier (BBB); however, IRA-BBB interactions are poorly studied. Here, we examined the [...] Read more.
Incretin receptor agonists (IRAs) such as GLP-1-based therapies improve metabolic and cognitive outcomes and enhance brain insulin signaling. One way that IRAs could have these actions is by affecting the blood–brain barrier (BBB); however, IRA-BBB interactions are poorly studied. Here, we examined the ability of insulin and IRAs to affect each other’s transport across the BBB in lean mice. We found that intracerebroventricular (ICV) administration of the insulin receptor antagonist S961 did not affect the blood-to-brain transport of the bioactive fragment of the IRA, 125I-dulaglutide (BAF). In contrast, 125I-dulaglutide (BAF) co-administered with intravenous (IV) insulin significantly enhanced 125I-dulaglutide (BAF) BBB transport into whole brain, olfactory bulb, parietal cortex, and pons, demonstrating insulin-dependent modulation of IRA BBB transport. Regional transport rates for 125I-dulaglutide (BAF) across the brain varied by ~2.5-fold, with the fastest transport into the olfactory bulb, frontal cortex, cerebellum, and pons. Co-administration of IV dulaglutide (BAF) did not alter 125I-insulin BBB transport rates (Ki) but did reduce reversible insulin binding (Vi) at the BBB by >50%, suggesting rapid effects on BBB insulin receptors. To explore the effects of chronic IRA administration, lean mice were treated with semaglutide for two weeks. Body weight and food intake were unchanged, but female mice showed reduced fasting levels of serum insulin and GLP-1 and decreased insulin transport into whole brain, while male mice showed a reduction in insulin binding at the BBB. Chronic semaglutide also reduced 125I-insulin BBB transport in female mice when studied with in situ perfusion, a procedure that removes the immediate influence of serum factors. Together, these findings demonstrate reciprocal and female-selective interactions between IRAs and insulin at the BBB. Acute insulin enhances the BBB transport of an IRA in female mice, whereas chronic IRA exposure selectively impairs insulin BBB transport in females, highlighting the BBB as a dynamic and hormone-sensitive interface with implications for long-term treatment in mouse models and potential for translation impact in humans. Full article
(This article belongs to the Special Issue Unveiling Molecular Mysteries of Brain Barriers)
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14 pages, 38911 KB  
Brief Report
Acute Seizure Susceptibility and Chronic Vascular Malformation in a Developmental Mouse Model of Sturge–Weber Syndrome
by Nicholas Truver, Chase Solomon and Anne Comi
Int. J. Mol. Sci. 2026, 27(8), 3519; https://doi.org/10.3390/ijms27083519 - 15 Apr 2026
Viewed by 587
Abstract
Sturge–Weber Syndrome (SWS) is a rare neurovascular disorder caused by a somatic mosaic missense point mutation in GNAQ, resulting in a facial capillary malformation (port-wine birthmark) and abnormal blood vessels in the eye and brain. Symptoms include seizures, stroke-like episodes, and glaucoma. Acute [...] Read more.
Sturge–Weber Syndrome (SWS) is a rare neurovascular disorder caused by a somatic mosaic missense point mutation in GNAQ, resulting in a facial capillary malformation (port-wine birthmark) and abnormal blood vessels in the eye and brain. Symptoms include seizures, stroke-like episodes, and glaucoma. Acute seizures induced with low-dose kainate in a transgenic GNAQ R183Q mouse model of SWS assessed seizure susceptibility and the impact of seizures on cerebral vasculature. Mice expressing human GNAQ mutation experienced more severe seizures and greater seizure-induced mortality compared to littermate controls. Mutant mice had longer cortical microvessels, with larger diameters; the expression of tight junction proteins was reduced 2 days after seizures. Blood–brain barrier permeability was not different from controls after chronic gene expression, although vascular dilation persisted compared to controls. These data demonstrate increased seizure susceptibility in this somatic mosaic model of SWS, bidirectional interactions between seizure and vascular remodeling, and chronic persistence of vascular malformation. Full article
(This article belongs to the Special Issue Unveiling Molecular Mysteries of Brain Barriers)
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