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Blood-Brain Barrier in Neuroinflammation and Neurological Diseases

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: 20 September 2024 | Viewed by 658

Special Issue Editor


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Guest Editor
Department of Neurology and Clinical Neuroscience, Graduate School of Medicine, Yamaguchi University, Ube 755-8505, Japan
Interests: neuroimmune disease; blood-brain barrier; blood-nerve barrier

Special Issue Information

Dear Colleagues,

The blood-brain barrier (BBB) plays a role as a structural and functional barrier that restricts the passage of soluble mediators and leukocytes from the blood to the central nervous system (CNS). Breakdown of the BBB is the key feature in several neuroimmunological diseases, including multiple sclerosis, neuromyelitis optica, collagen disease and autoimmune encephalitis. In addition, dysfunction of BBB is also noted in various neurological diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, trauma, diabetes, hypertension, cerebral small vessel disease and neuropathic pain. However, optimal treatment targeting the BBB has not been yet developed.

This Special Issue aims to focus on both basic molecular science and translational research on the blood-brain barrier in neuroinflammation and neurological diseases. We invite submissions of manuscripts related to the establishment of new BBB in vitro/in vivo models, pathological observation of BBB, or new diagnostic biomarkers of BBB breakdown in these diseases, the blood-nerve barrier and bloodCSF barrier. Review articles on the BBB highlighting the pathomechanisms and treatment strategies in these diseases will also be accepted.

Dr. Fumitaka Shimizu
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 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • blood-brain barrier
  • in vitro model
  • in vivo model
  • pathology
  • blood–spinal cord barrier
  • blood–CSF barrier
  • blood–nerve barrier
  • multiple sclerosis
  • neuromyelitis optica
  • Alzheimer’s disease
  • Parkinson’s disease
  • collagen disease
  • autoimmune encephalitis
  • amyotrophic lateral sclerosis
  • trauma
  • diabetes
  • cerebral small vessel disease
  • neuropathic pain
  • autoimmune neuropathy

Published Papers (1 paper)

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Research

15 pages, 1932 KiB  
Article
The Blood–Brain Barrier Is Unaffected in the Ndufs4−/− Mouse Model of Leigh Syndrome
by Robin Reynaud-Dulaurier, Romain Clément, Sara Yjjou, Cassandra Cresson, Yasmina Saoudi, Mathilde Faideau and Michael Decressac
Int. J. Mol. Sci. 2024, 25(9), 4828; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25094828 - 29 Apr 2024
Viewed by 307
Abstract
Mitochondrial dysfunction plays a major role in physiological aging and in many pathological conditions. Yet, no study has explored the consequence of primary mitochondrial deficiency on the blood–brain barrier (BBB) structure and function. Addressing this question has major implications for pharmacological and genetic [...] Read more.
Mitochondrial dysfunction plays a major role in physiological aging and in many pathological conditions. Yet, no study has explored the consequence of primary mitochondrial deficiency on the blood–brain barrier (BBB) structure and function. Addressing this question has major implications for pharmacological and genetic strategies aimed at ameliorating the neurological symptoms that are often predominant in patients suffering from these conditions. In this study, we examined the permeability of the BBB in the Ndufs4−/− mouse model of Leigh syndrome (LS). Our results indicated that the structural and functional integrity of the BBB was preserved in this severe model of mitochondrial disease. Our findings suggests that pharmacological or gene therapy strategies targeting the central nervous system in this mouse model and possibly other models of mitochondrial dysfunction require the use of specific tools to bypass the BBB. In addition, they raise the need for testing the integrity of the BBB in complementary in vivo models. Full article
(This article belongs to the Special Issue Blood-Brain Barrier in Neuroinflammation and Neurological Diseases)
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