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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 (2nd Edition)

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

Deadline for manuscript submissions: 28 February 2025 | Viewed by 4279

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

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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.

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Keywords

  • blood cells
  • plasma components
  • vascular wall components
  • neurovascular unit
  • neuroinflammation
  • cognitive decline

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Related Special Issue

Published Papers (3 papers)

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Research

18 pages, 14132 KiB  
Article
Retinal Vascular and Structural Changes in the Murine Alzheimer’s APPNL-F/NL-F Model from 6 to 20 Months
by Lidia Sánchez-Puebla, Inés López-Cuenca, Elena Salobrar-García, María González-Jiménez, Alberto Arias-Vázquez, José A. Matamoros, Ana I. Ramírez, José A. Fernández-Albarral, Lorena Elvira-Hurtado, Takaomi C. Saido, Takashi Saito, Carmen Nieto-Vaquero, María I. Cuartero, María A. Moro, Juan J. Salazar, Rosa de Hoz and José M. Ramírez
Biomolecules 2024, 14(7), 828; https://doi.org/10.3390/biom14070828 - 10 Jul 2024
Viewed by 1338
Abstract
Alzheimer’s disease (AD) may manifest retinal changes preceding brain pathology. A transversal case-control study utilized spectral-domain OCT angiography (SD-OCTA) and Angio-Tool software 0.6a to assess retinal vascular structures and OCT for inner and outer retina thickness in the APPNL-F/NL-F AD model at [...] Read more.
Alzheimer’s disease (AD) may manifest retinal changes preceding brain pathology. A transversal case-control study utilized spectral-domain OCT angiography (SD-OCTA) and Angio-Tool software 0.6a to assess retinal vascular structures and OCT for inner and outer retina thickness in the APPNL-F/NL-F AD model at 6, 9, 12, 15, 17, and 20 months old. Comparisons to age-matched wild type (WT) were performed. The analysis focused on the three vascular plexuses using AngiooTool and on retinal thickness, which was represented with the Early Treatment Diabetic Retinopathy Study (ETDRS) sectors. Compared to WT, the APPNL-F/NL-F group exhibited both vascular and structural changes as early as 6 months persisting and evolving at 15, 17, and 20 months. Significant vascular alterations, principally in the superficial vascular complex (SVC), were observed. There was a significant decrease in the vessel area and the total vessel length in SVC, intermediate, and deep capillary plexus. The inner retina in the APPNL-F/NL-F group predominantly decreased in thickness while the outer retina showed increased thickness in most analyzed time points compared to the control group. There are early vascular and structural retinal changes that precede the cognitive changes, which appear at later stages. Therefore, the natural history of the APPNL-F/NL-F model may be more similar to human AD than other transgenic models. Full article
(This article belongs to the Special Issue The Role of Vascular Dysfunction in Neuronal Degeneration and Cognitive Impairment (2nd Edition))
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9 pages, 267 KiB  
Article
Endothelial Dysfunction and Pre-Existing Cognitive Disorders in Stroke Patients
by Anne-Marie Mendyk-Bordet, Thavarak Ouk, Anne Muhr-Tailleux, Maud Pétrault, Emmanuelle Vallez, Patrick Gelé, Thibaut Dondaine, Julien Labreuche, Dominique Deplanque and Régis Bordet
Biomolecules 2024, 14(6), 721; https://doi.org/10.3390/biom14060721 - 18 Jun 2024
Viewed by 775
Abstract
Background: The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis. Objective: To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients. Methods: Patients originated from [...] Read more.
Background: The origin of pre-existing cognitive impairment in stroke patients remains controversial, with a vascular or a degenerative hypothesis. Objective: To determine whether endothelial dysfunction is associated with pre-existing cognitive problems, lesion load and biological anomalies in stroke patients. Methods: Patients originated from the prospective STROKDEM study. The baseline cognitive state, assessed using the IQ-CODE, and risk factors for stroke were recorded at inclusion. Patients with an IQ-CODE score >64 were excluded. Endothelial function was determined 72 h after stroke symptom onset by non-invasive digital measurement of endothelium-dependent flow-mediated dilation and calculation of the reactive hyperemia index (RHI). RHI ≤ 1.67 indicated endothelial dysfunction. Different biomarkers of endothelial dysfunction were analysed in blood or plasma. All patients underwent MRI 72 h after stroke symptom onset. Results: A total of 86 patients were included (52 males; mean age 63.5 ± 11.5 years). Patients with abnormal RHI have hypertension or antihypertensive treatment more often. The baseline IQ-CODE was abnormal in 33 (38.4%) patients, indicating a pre-existing cognitive problem. Baseline IQ-CODE > 48 was observed in 15 patients (28.3%) with normal RHI and in 18 patients (54.6%) with abnormal RHI (p = 0.016). The RHI median was significantly lower in patients with abnormal IQ-CODE. Abnormal RHI was associated with a significantly higher median FAZEKAS score (2.5 vs. 2; p = 0.008), a significantly higher frequency of periventricular lesions (p = 0.015), more white matter lesions (p = 0.007) and a significantly higher cerebral atrophy score (p < 0.001) on MRI. Vascular biomarkers significantly associated with abnormal RHI were MCP-1 (p = 0.009), MIP_1a (p = 0.042), and homocysteinemia (p < 0.05). Conclusions: A vascular mechanism may be responsible for cognitive problems pre-existing stroke. The measurement of endothelial dysfunction after stroke could become an important element of follow-up, providing an indication of the functional and cognitive prognosis of stroke patients. Full article
(This article belongs to the Special Issue The Role of Vascular Dysfunction in Neuronal Degeneration and Cognitive Impairment (2nd Edition))
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 1569
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 (2nd Edition))
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