Recent Advances in Brain Vascular Diseases Management and Therapy 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 2711

Special Issue Editor

Special Issue Information

Dear Colleagues,

Brain plasticity allows for the continuous remodeling of the brain’s structure and function during aging and disease. Aging is accompanied by changes in blood vessel structure, leading to a decrease in blood flow to the peripheral organs. In the central nervous system, cerebral vascular aging can lead to a loss of the integrity of the blood-brain barrier, eventually resulting in cognitive and sensorimotor decline. One of the major of types of cognitive dysfunction due to chronic cerebral hypoperfusion is vascular cognitive impairment and degenerative processes that lead to dementia. Thus, some patients suffering from Alzheimer’s disease present with symptoms manifested by cortical and/or subcortical clinical symptoms that are related to the atheromatous vascular degeneration of the brain’s arteries.

Thus, comprehensive approaches need to be developed that address the multiple, interrelated mechanisms of brain aging. Attention is drawn to the importance of the maintenance of cerebromicrovascular health; the restoration of neuroendocrine balance; and the pressing need for funding more innovative research into the interactions between neuronal, neuroendocrine, inflammatory, and microvascular mechanisms in cognitive impairment and Alzheimer’s disease.

Old age in both humans and animals is associated with an enhanced susceptibility to stroke; aged animals recover poorly from brain injuries compared to young rodents. Stroke increases the risk of cognitive impairment and dementia and may contribute to the progression of Alzheimer's disease. 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.

During the past several years, there has been increasing interest in the role of human cerebrovasculature and the blood-brain barrier (BBB) as etiological factors contributing to the development of seizures and chronic epilepsy. Recently, much emphasis has been placed on dysregulated angiogenesis, BBB permeability, and epilepsy.

This Special Issue of Biomedicines will provide up-to-date information on different aspects of brain aging from the latest developments in the field of neurodegenerative disorders to cerebral microvascular mechanisms of cognitive decline. New avenues for research targeting cellular senescence, epigenetics, and endocrine mechanisms of brain aging are also discussed. Based on the current literature, it is clear that understanding brain aging and reducing the risk of neurological disease with age requires searching for mechanisms and treatment options beyond age-related changes in neuronal function. This Special Issue will also cover recent advances in brain vasculature in signaling pathways that can potentially protect cells, as well as treatment options for the maintenance of cerebromicrovascular functioning to prevent diseases associated with brain vasculature remodeling in response to aging and associated diseases and present new treatment options.

Prof. Dr. Aurel Popa-Wagner
Guest Editor

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Keywords

  • aging
  • vasculature
  • cognition
  • dementia
  • stroke
  • hemorrhagic stroke
  • comorbidities
  • epilepsy
  • Alzheimer’s disease

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Published Papers (1 paper)

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Research

20 pages, 5876 KiB  
Article
Neuroprotective Effects of Human-Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cell Extracellular Vesicles in Ischemic Stroke Models
by Gang Lu, Xianwei Su, Lihong Wang, Chi-Kwan Leung, Jingye Zhou, Zhiqiang Xiong, Wuming Wang, Hongbin Liu and Wai-Yee Chan
Biomedicines 2023, 11(9), 2550; https://doi.org/10.3390/biomedicines11092550 - 17 Sep 2023
Cited by 5 | Viewed by 2235
Abstract
Background: Stroke represents the second leading cause of death and the primary cause of long-term disability in humans. The transplantation of mesenchymal stem cells (MSC) reportedly improves functional outcomes in animal models of cerebral ischemia. Here, we evaluate the neuroprotective potential of extracellular [...] Read more.
Background: Stroke represents the second leading cause of death and the primary cause of long-term disability in humans. The transplantation of mesenchymal stem cells (MSC) reportedly improves functional outcomes in animal models of cerebral ischemia. Here, we evaluate the neuroprotective potential of extracellular vesicles secreted from human-induced pluripotent stem cell-derived mesenchymal stem cells (hiPS-MSC-EV) using preclinical cell-based and animal-based models of ischemic strokes. Methods: hiPS-MSC-EV were isolated using an ultrafiltration method. HT22 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury for 2 h, followed by treatment with hiPS-MSC-EV (100 μg/mL). Male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO) followed by an intravenous injection of hiPS-MSC-EV (100 μg) at three distinct time points. Results: Our experimental approach revealed hiPS-MSC-EV promoted HT22 cell proliferation, reduced apoptosis, and altered cellular morphology following OGD/R. In addition, hiPS-MSC-EV reduced the volume of infarcts, improved spontaneous movement abilities, and enhanced angiogenesis by expressing the VEGF and CXCR4 proteins in the infarcted hemisphere of the MCAO-treated mouse model. Conclusion: Our findings provide evidence of the potential neuroprotective effects of hiPS-MSC-derived extracellular vesicles (hiPS-MSC-EVs) in both in vitro and in vivo mouse models of ischemic stroke. These results suggest that hiPS-MSC-EVs may play a role in neurorestoration and offer insights into potential cell-free strategies for addressing cerebral ischemia. Full article
(This article belongs to the Special Issue Recent Advances in Brain Vascular Diseases Management and Therapy 2.0)
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