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Biomolecules
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The Role of Vascular Dysfunction in Neuronal Degeneration and Cognitive...
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The Role of Vascular Dysfunction in Neuronal Degeneration and Cognitive Impairment 2.0

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1186

Special Issue Editor

Prof. Dr. David Lominadze

E-Mail Website
Guest Editor
1. Department of Surgery, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
2. Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA
Interests: microcirculation; cerebrovascular permeability; extravascular deposition of fibrinogen; formation of fibrinogen and other protein complexes; role of activated astrocytes in neurodegeneration; traumatic brain injury
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegeneration inevitably leads to cognitive impairment significantly altering quality of life of affected people. Neuroinflammatory diseases such as Alzheimer’s disease (AD), multiple sclerosis (MS), traumatic brain injury (TBI), and stroke are associated with memory reduction caused by impairment of neuronal function. During the past decade greater attention has been given to vascular effects involved in cognitive decline. The topic of vascular cognitive impairment and dementia has been identified as one of the research priorities by the NIH. Many of these neuroinflammatory responses are associated with changes in systemic circulation and brain vasculature. Various mechanisms involved neurodegeneration and cognitive decline originated in vasculature have been identified and validated. However, many more questions still remain. The main reason for this can be a functional complexity of neuro-vascular unit and number of cells that can affect vasculo-neuronal interactions during various neuroinflammatory and neurodegenerative diseases.  

Based on success of our first edition, this second edition of the Special Issue is to gather original findings and intriguing hypothesis related to alterations in vasculature, blood, their components, and their function that can result in neurodegeneration and lead to cognitive decline. It should be noted that this Special Issue will consider publication of original research articles as well as review articles.

Prof. Dr. David Lominadze
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.

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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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 cells
  • plasma components
  • vascular wall components
  • neurovascular unit
  • neuroinflammation
  • cognitive decline

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Published Papers (1 paper)

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Research

13 pages, 2329 KiB  
Article
The Effect of Reduced Fibrinogen on Cerebrovascular Permeability during Traumatic Brain Injury in Fibrinogen Gene Heterozygous Knockout Mice
by Nurul Sulimai, Jason Brown and David Lominadze
Biomolecules 2024, 14(4), 385; https://doi.org/10.3390/biom14040385 - 22 Mar 2024
Viewed by 843
Abstract
Vascular contribution to cognitive impairment and dementia (VCID) is a term referring to all types of cerebrovascular and cardiovascular disease-related cognitive decline, spanning many neuroinflammatory diseases including traumatic brain injury (TBI). This becomes particularly important during mild-to-moderate TBI (m-mTBI), which is characterized by [...] Read more.
Vascular contribution to cognitive impairment and dementia (VCID) is a term referring to all types of cerebrovascular and cardiovascular disease-related cognitive decline, spanning many neuroinflammatory diseases including traumatic brain injury (TBI). This becomes particularly important during mild-to-moderate TBI (m-mTBI), which is characterized by short-term memory (STM) decline. Enhanced cerebrovascular permeability for proteins is typically observed during m-mTBI. We have previously shown that an increase in the blood content of fibrinogen (Fg) during m-mTBI results in enhanced cerebrovascular permeability. Primarily extravasated via a transcellular pathway, Fg can deposit into the parenchyma and exacerbate inflammatory reactions that can lead to neurodegeneration, resulting in cognitive impairment. In the current study, we investigated the effect of a chronic reduction in Fg concentration in blood on cerebrovascular permeability and the interactions of extravasated Fg with astrocytes and neurons. Cortical contusion injury (CCI) was used to generate m-mTBI in transgenic mice with a deleted Fg γ chain (Fg γ+/−), resulting in a low blood content of Fg, and in control C57BL/6J wild-type (WT) mice. Cerebrovascular permeability was tested in vivo. Interactions of Fg with astrocytes and neurons and the expression of neuronal nuclear factor-кB (NF-кB) were assessed via immunohistochemistry. The results showed that 14 days after CCI, there was less cerebrovascular permeability, lower extravascular deposition of Fg, less activation of astrocytes, less colocalization of Fg with neurons, and lower expression of neuronal pro-inflammatory NF-кB in Fg γ+/− mice compared to that found in WT mice. Combined, our data provide strong evidence that increased Fg extravasation, and its resultant extravascular deposition, triggers astrocyte activation and leads to potential interactions of Fg with neurons, resulting in the overexpression of neuronal NF-кB. These effects suggest that reduced blood levels of Fg can be beneficial in mitigating the STM reduction seen in m-mTBI. Full article
(This article belongs to the Special Issue The Role of Vascular Dysfunction in Neuronal Degeneration and Cognitive Impairment 2.0)
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