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Stroke Life Style: Advancing Our Understanding of Disease Mechanism and Therapy

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Vascular Medicine".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 11451

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Special Issue Editor

Prof. Dr. Aurel Popa-Wagner

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Guest Editor

Department of Neurology, University of Medicine Essen, Essen, Germany
Interests: ageing; cerebrovascular diseases; cell therapies; gene therapy; behavioral recovery; genomics; proteomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Old age is associated with an enhanced susceptibility to stroke, and aged animals recover poorly from brain injuries as compared to young rodents. Despite the initial hope that cell-based therapies may stimulate restorative processes in the ischemic brain, it is now recognized that aging processes may promote an unfavorable environment for such treatments. Virtually all drug interventions that have been successful preclinically in experimental stroke have failed to translate this success to the clinical setting. The failure to consider the complexity and heterogeneity of human diseases and co-morbidities may render neuroprotective drugs less efficacious in clinical practice. It is becoming evident that subtle but continuous neuroinflammation can provide the ground for disorders such as cerebral small vessel disease (cSVD) and subsequently dementia. Moreover, advanced aging and a number of highly prevalent risk factors such as obesity hypertension, diabetes, and atherosclerosis are increasingly understood to act as “silent contributors” to neuroinflammation—not only establishing the condition as a central pathophysiological mechanism, but also constantly fueling it. Acute neuroinflammation, often in the context of traumatic or ischemic CNS lesions, aggravates the acute damage and can lead to a number of pathological illnesses, such as depression, post-stroke dementia and potentially neurodegeneration. All of those sequelae impair recovery and most of them provide the ground for further cerebrovascular events; thus, a vicious cycle develops. We also cover brain vasculature recent advances in signaling pathways that can potentially protect cells as well as treatment options for the maintenance of brain capillaries to prevent diseases associated with brain vasculature remodeling in response to aging and associated comorbidities.

This Special Issue of JCM will provide an up-to-date information on molecular, cellular, and behavioral events associated with stroke epidemiology and new therapeutic options for treatment options.

Prof. Dr. Aurel Popa-Wagner
Guest Editor

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Keywords

aging
stroke, epidemiology
co-morbidities
hyperlipidemia
diabetes
hypertension
treatment

Published Papers (4 papers)

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Research

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12 pages, 2422 KiB

Open AccessArticle

Monomeric C-Reactive Protein Aggravates Secondary Degeneration after Intracerebral Haemorrhagic Stroke and May Function as a Sensor for Systemic Inflammation

by Mark Slevin, Elisa García-Lara, Bogdan Capitanescu, Coral Sanfeliu, Yasmin Zeinolabediny, Raid AlBaradie, Peter Olah, Baoqiang Guo, Daniel Pirici, Mario Di Napoli and Aurel Popa-Wagner

J. Clin. Med. 2020, 9(9), 3053; https://doi.org/10.3390/jcm9093053 - 22 Sep 2020

Cited by 18 | Viewed by 2834

Abstract

Background: We previously identified increased tissue localization of monomeric C-reactive protein (mCRP) in the infarcted cortical brain tissue of patients following ischaemic stroke. Here, we investigated the relationship of mCRP expression in haemorrhagic stroke, and additionally examined the capacity of mCRP to travel to or appear at other locations within the brain that might account for later chronic neuroinflammatory or neurodegenerative effects. Methods: Immunohistochemistry was performed on Formalin-fixed, paraffin-embedded archived brain tissue blocks obtained at autopsy from stroke patients and age-matched controls. We modelled mCRP migration into the brain after haemorrhagic stroke by infusing mCRP (3.5 µg) into the hippocampus of mice and localized mCRP with histological and immunohistochemistry methods. Results: On human tissue in the early stages of haemorrhage, there was no staining of mCRP. However, with increasing post-stroke survival time, mCRP immunostaining was associated with some parenchymal brain cells, some stroke-affected neurons in the surrounding areas and the lumen of large blood vessels as well as brain capillaries. Further from the peri-haematoma region, however, mCRP was detected in the lumen of micro-vessels expressing aquaporin 4 (AQP4). In the hypothalamus, we detected clusters of neurons loaded with mCRP along with scattered lipofuscin-like deposits. In the peri-haematoma region of patients, mCRP was abundantly seen adjacent to AQP4 immunoreactivity. When we stereotactically injected mCRP into the hippocampus of mice, we also observed strong expression in distant neurones of the hypothalamus as well as cortical capillaries. Conclusions: mCRP is abundantly expressed in the brain after haemorrhagic stroke, directly impacting the pathophysiological development of the haematoma. In addition, it may have indirect effects, where the microcirculatory system appears to be able to carry it throughout the cortex as far as the hypothalamus, allowing for long-distance effects and damage through its capacity to induce inflammation and degenerate neuronal perivascular compartments. Full article

(This article belongs to the Special Issue Stroke Life Style: Advancing Our Understanding of Disease Mechanism and Therapy)

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10 pages, 572 KiB

Open AccessArticle

Association of Hypertensive Intracerebral Hemorrhage with Left Ventricular Hypertrophy on Transthoracic Echocardiography

by Lars-Peder Pallesen, Jenny Wagner, Dimitris Lambrou, Silke Braun, Matthias Weise, Alexandra Prakapenia, Jessica Barlinn, Timo Siepmann, Simon Winzer, Haidar Moustafa, Hagen H. Kitzler, Kristian Barlinn, Heinz Reichmann and Volker Puetz

J. Clin. Med. 2020, 9(7), 2148; https://doi.org/10.3390/jcm9072148 - 08 Jul 2020

Cited by 8 | Viewed by 1934

Abstract

Introduction: Arterial hypertension is the most frequent cause for spontaneous intracerebral hemorrhage (sICH) and may also cause left ventricular hypertrophy (LVH). We sought to analyze whether hypertensive sICH etiology is associated with LVH. Methods: We analyzed consecutive patients with sICH who were admitted to our tertiary stroke center during a four-year period and underwent transthoracic echocardiography (TTE) as part of the diagnostic work-up. We defined hypertensive sICH as typical localization of hemorrhage in patients with arterial hypertension and no other identified sICH etiology. We defined an increased end-diastolic interventricular septal wall thickness of ≥11 mm on TTE as a surrogate parameter for LVH. Results: Among 395 patients with sICH, 260 patients (65.8%) received TTE as part of their diagnostic work-up. The median age was 71 years (interquartile range (IQR) 17), 160 patients (61.5%) were male, the median baseline National Institute of Health Stroke Scale (NIHSS) score was 8 (IQR 13). Of these, 159 (61.2%) patients had a hypertensive sICH and 156 patients (60%) had LVH. In univariable (113/159 (71.1%) vs. 43/101 (42.6%); odds ratio (OR) 3.31; 95% confidence interval (CI_95%) 1.97–5.62); and multivariable (adjusted OR 2.95; CI_95% 1.29–6.74) analysis, hypertensive sICH was associated with LVH. Conclusions: In patients with sICH, LVH is associated with hypertensive bleeding etiology. Performing TTE is meaningful for diagnosis of comorbidities and clarification of bleeding etiology in these patients. Future studies should include long-term outcome parameters and assess left ventricular mass as main indicator for LVH. Full article

(This article belongs to the Special Issue Stroke Life Style: Advancing Our Understanding of Disease Mechanism and Therapy)

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18 pages, 1017 KiB

Open AccessArticle

Gender Differences in the Levels of Periodontal Destruction, Behavioral Risk Factors and Systemic Oxidative Stress in Ischemic Stroke Patients: A Cohort Pilot Study

by Ioana Stănescu, Adriana Elena Bulboacă, Iulia Cristina Micu, Sorana D. Bolboacă, Dana Gabriela Feștilă, Angelo C. Bulboacă, Gyorgy Bodizs, Gabriela Dogaru, Paul Mihai Boarescu, Aurel Popa-Wagner and Alexandra Roman

J. Clin. Med. 2020, 9(6), 1744; https://doi.org/10.3390/jcm9061744 - 04 Jun 2020

Cited by 8 | Viewed by 2511

Abstract

Background: Due to the higher frequency of ischemic stroke in men compared to women, we aimed to determine if gender differences exist regarding periodontal status and several plasma biomarkers in patients with a recent large artery atherosclerosis ischemic stroke (IS). Material and methods: Patients with their first IS within less than six weeks who were able to undergo periodontal examinations were evaluated. Demographic data, periodontal status, oxidative stress parameters/plasma antioxidant capacity, and C-reactive protein in patients who suffered a recent large artery atherosclerosis ischemic stroke were reccorded. Results: 93 patients were included in the study. More men were smokers (12/57 vs. 3/36) and consumed alcohol (17/57 vs. 3/36), and more women had higher glycemic values (p = 0.023), total cholesterol (p < 0.001), LDL (low-density lipoprotein)-cholesterol (p = 0.010), and HDL (high-density lipoprotein)-cholesterol (p = 0.005) levels. Significantly more men than women had moderate plus severe periodontal disease (p = 0.018), significantly higher levels of nitric oxide (p = 0.034), and significantly lower levels of total antioxidant capacity (p = 0.028). Conclusions: In this pilot study, men seem to be more prone to oxidative stress and to develop more severe forms of periodontitis among patients with stroke, but the results need validation on a larger sample. Full article

(This article belongs to the Special Issue Stroke Life Style: Advancing Our Understanding of Disease Mechanism and Therapy)

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Review

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18 pages, 1323 KiB

Open AccessReview

Roles of Microglial Ion Channel in Neurodegenerative Diseases

by Alexandru Cojocaru, Emilia Burada, Adrian-Tudor Bălșeanu, Alexandru-Florian Deftu, Bogdan Cătălin, Aurel Popa-Wagner and Eugen Osiac

J. Clin. Med. 2021, 10(6), 1239; https://doi.org/10.3390/jcm10061239 - 17 Mar 2021

Cited by 11 | Viewed by 3584

Abstract

As the average age and life expectancy increases, the incidence of both acute and chronic central nervous system (CNS) pathologies will increase. Understanding mechanisms underlying neuroinflammation as the common feature of any neurodegenerative pathology, we can exploit the pharmacology of cell specific ion channels to improve the outcome of many CNS diseases. As the main cellular player of neuroinflammation, microglia play a central role in this process. Although microglia are considered non-excitable cells, they express a variety of ion channels under both physiological and pathological conditions that seem to be involved in a plethora of cellular processes. Here, we discuss the impact of modulating microglia voltage-gated, potential transient receptor, chloride and proton channels on microglial proliferation, migration, and phagocytosis in neurodegenerative diseases. Full article

(This article belongs to the Special Issue Stroke Life Style: Advancing Our Understanding of Disease Mechanism and Therapy)

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