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Users are allowed to share and adapt the chapters for any non-commercial purposes as long as the authors and the publisher are explicitly identified and properly acknowledged as the original source. The books in their entirety are subject to copyright by the publisher. The reproduction, modification, republication and display of the books in their entirety, in any form, by anyone, for commercial purposes are strictly prohibited without the written consent of the publisher.</p> Front Matter https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-front-matter CEREBRAL ISCHEMIA Ryszard Pluta, MD, PhD (Editor) Copyright (c) 2021 Exon Publications https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 10.36255/exonpublications.cerebralischemia.2021.frontmatter Foreword https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-foreword <p>Post-ischemic brain damage is one of the leading causes of death worldwide, resulting in increased disability that significantly impacts patients’ quality of life, healthcare costs, and resource use. The incidence of cerebral ischemia increases with age, and it is estimated that about 20% of cases occur in young people between the ages of 18 and 50. The incidence of cerebral ischemia has increased in the younger population under the age of 55, especially in Europe and the United States. However, in the elderly population, the risk of cerebral ischemia is 1 in 3. Currently, approximately 17 million patients each year suffer from ischemic brain injury, of which 6 million will die. In addition, long-term complications, such as the development of dementia, can affect up to half of all survivors of cerebral ischemia and they can live with the debilitating consequences of ischemia for more than twenty years. Recently, significant advances in knowledge of cerebral ischemia have been observed through the use of proteomic and genomic tools in laboratory studies of post-ischemic brain neurodegeneration with the Alzheimer’s disease phenotype and genotype. In clinical and experimental studies following cerebral ischemia, a characteristic neuropathology of Alzheimer’s disease was found, including diffuse and senile amyloid plaques and pathology of the tau protein. <a href="https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-foreword/807">CONTINUE READING.....</a></p> Janusz Kocki, MD, PHD Copyright (c) 2021 Exon Publications https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 vii vii 10.36255/exonpublications.cerebralischemia.2021.foreword Preface https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-preface <p>Cerebral ischemia is a global public health threat and one of the important causes of mortality and loss of independence in those affected. Moreover, cerebral ischemia is one of the most common causes of dementia, which sooner or later develops in more than half of patients after an ischemic episode. This book presents a new picture of ischemic brain disease that knows no geographic boundaries and continues to attract the attention of a large community of scientists, physicians, engineers, and related health professionals by synthesizing the latest modern data on disease progression mechanisms and possible care for patients with this disease. The authors present the characteristics of cerebral ischemia from pregnancy and childhood through adolescence to adulthood. Post-ischemic brain injury in animals and humans leads to proteomic, genomic, and structural changes in various brain structures, starting in the hippocampus, showing changes identical to those seen in Alzheimer’s disease. Cerebral ischemia is the second naturally occurring disease after Alzheimer’s disease, which primarily causes the death of pyramidal neurons in the CA1 region of the hippocampus. The main pathology is considered to be post-ischemic changes in the hippocampus, especially in its CA1 area, underlying episodic memory impairment, which is the earliest and most important clinical symptom of post-ischemic dementia. <a href="https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-preface/808">CONTINUE READING…..</a></p> Ryszard Pluta, MD, PHD Copyright (c) 2021 Exon Publications https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 ix x 10.36255/exonpublications.cerebralischemia.2021.preface Contributors https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-contributors <p><strong>AGATA TARKOWSKA, MD, PHD</strong><br>Department of Neonate and Infant Pathology, Medical University of Lublin, Lublin, Poland</p> <p><strong>AIKO OSAWA, MD, PHD</strong><br>Department of Rehabilitation Medicine, National Center for Geriatrics and Gerontology, Aichi, Japan</p> <p><strong>ALEJANDRO GARCIA-RUDOLPH, PHD</strong><br>Department of Research and Innovation, Institut Guttmann, Institut Universitari de Neurorehabilitació Adscrit a la UAB, Badalona, Spain</p> <p><strong>ASHISH RATHAWA, MBBS, MS</strong><br>Department of Anatomy, GMERS Medical College, Junagadh, Gujarat, India</p> <p><strong>AYMAN ELALI, PHD</strong><br>Department of Psychiatry and Neuroscience, Faculty of Medicine, Université Laval, Quebec City, QC, Canada</p> <p><strong>BHAKTA PRASAD GAIRE, PHD</strong><br>Department of Anesthesiology and Neurology, Shock Trauma and Anesthesiology Research Center, University of Maryland, School of Medicine, Baltimore, MD, USA</p> <p><strong>BINGREN HU, PHD</strong><br>Department of Anesthesiology and Neurology, Shock Trauma and Anesthesiology Research Center, University of Maryland, School of Medicine, Baltimore, MD, USA</p> <p><strong>DAGMAR KALENSKA, PHD</strong><br>Department of Anatomy, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>DANIEL MANRIQUE-CASTANO, PHD</strong><br>Neuroscience Axis, Research Center of CHU de Québec - Université Laval, Québec City, QC, Canada</p> <p><strong>DARKO LOVIĆ, MPHARM</strong><br>Center for Laser Microscopy, Faculty of Biology, University of Belgrade, Serbia</p> <p><strong>EVA BARANOVICOVA, PHD</strong><br>BioMed Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>GIRISH CHAUHAN, BDS, MDS</strong><br>Department of Oral Pathology, Government Dental College, Jamanagar, Gujarat, India</p> <p><strong>HIRONORI TERAMOTO, BSC</strong><br>Department of Anesthesiology and Neurology, Shock Trauma and Anesthesiology Research Center, University of Maryland, School of Medicine, Baltimore, MD, USA</p> <p><strong>JAN LEHOTSKY, PHD, DSC</strong><br>Department of Medical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>JOAN SAURÍ, PHD</strong><br>Department of Research and Innovation, Institut Guttmann, Institut Universitari de Neurorehabilitació Adscrit a la UAB, Badalona, Spain</p> <p><strong>JOHN D. KELLEHER, PHD</strong><br>ADAPT Research Centre, Technological University Dublin, Ireland</p> <p><strong>KATARINA ŽIVANČEVIĆ, MPHARM</strong><br>Center for Laser Microscopy, Faculty of Biology, University of Belgrade, Serbia</p> <p><strong>KATRYNA CISEK, PHD</strong><br>PRECISE4Q, Predictive Modelling in Stroke, Information Communications and Entertainment Institute, Technological University Dublin, Dublin, Ireland</p> <p><strong>KINJAL JETHWA, MBBS, MS</strong><br>Department of Anatomy, SKBS Medical College and Research Institute, Sumandeep Vidhyapeeth, Baroda, Gujarat, India</p> <p><strong>LALITA SUBEDI, PHD</strong><br>Department of Anesthesiology and Neurology, Shock Trauma and Anesthesiology Research Center, University of Maryland, School of Medicine, Baltimore, MD, USA</p> <p><strong>LARS TATENHORST, PHD</strong><br>Department of Neurology, University of Göttingen Medical School, Göttingen, Germany</p> <p><strong>LIDIJA RADENOVIĆ, PHD</strong><br>Center for Laser Microscopy, Faculty of Biology, University of Belgrade, Serbia</p> <p><strong>MARIA KOVALSKA, PHD</strong><br>Department of Histology and Embryology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>MARTA RUSEK, PHD</strong><br>Department of Pathophysiology, Medical University of Lublin, Lublin, Poland</p> <p><strong>MARZENA UŁAMEK-KOZIOŁ, MD, PHD</strong><br>Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland</p> <p><strong>MATHIAS BÄHR, MD</strong><br>Department of Neurology, University of Göttingen Medical School, Göttingen, Germany</p> <p><strong>MATTEO HAUPT, BSC</strong><br>Department of Neurology, University of Göttingen Medical School, Göttingen, Germany</p> <p><strong>MIROSŁAW JABŁOŃSKI, MD, PHD</strong><br>Department of Rehabilitation and Orthopaedics, Medical University of Lublin, Lublin, Poland</p> <p><strong>PAVLE R. ANDJUS, PHD</strong><br>Center for Laser Microscopy, Faculty of Biology, University of Belgrade, Serbia</p> <p><strong>PETER KAPLAN, PHD</strong><br>Department of Medical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>PETRA HNILICOVA, PHD</strong><br>BioMed Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Mala Hora, Martin, Slovakia</p> <p><strong>PRADIP CHAUHAN, MBBS, MS, CRM</strong><br>Department of Anatomy, All India Institute of Medical Sciences, Rajkot, Gujarat, India</p> <p><strong>RYSZARD PLUTA, MD, PHD</strong><br>Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland</p> <p><strong>SHINICHIRO MAESHIMA, MD, PHD</strong><br>Kinjo University, Ishikawa, Japan</p> <p><strong>SIMMI MEHRA, MBBS, MS</strong><br>Department of Anatomy, All India Institute of Medical Sciences, Rajkot, Gujarat, India</p> <p><strong>STANISŁAW J. CZUCZWAR, MD, PHD</strong><br>Department of Pathophysiology, Medical University of Lublin, Lublin, Poland</p> <p><strong>THI NGUYET QUE NGUYEN, PHD</strong><br>PRECISE4Q, Predictive Modelling in Stroke, Information Communications and Entertainment Institute, Technological University Dublin, Dublin, Ireland</p> <p><strong>THORSTEN R. DOEPPNER, MD, MSC</strong><br>Department of Neurology, University of Göttingen Medical School, Göttingen, Germany</p> <p><strong>XUAN ZHENG, MSC</strong><br>Department of Neurology, University of Göttingen Medical School, Göttingen, Germany</p> List of Contributors Copyright (c) 2021 Exon Publications https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 xi xiv 10.36255/exonpublications.cerebralischemia.2021.contributors The Anatomy of the Cerebral Cortex https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-cerebral-cortex <p>ABSTRACT</p> <p>The cerebral hemisphere consists of five lobes: frontal, parietal, temporal, occipital, and limbic lobe. Each cerebral hemisphere shows superomedial, inferior, and medial surfaces separated by superomedial, inferomedial, and inferolateral borders. The superolateral surface shows the central sulcus that separates the pre-central and post-central gyri. The parietal lobe is divided by the interparietal sulcus into supra-parietal and infra-parietal lobes. The occipital lobe contains the primary visual area surrounded by peristriate and parastriate areas. The temporal lobe is divided into superior, middle, and inferior temporal gyri. The superior surface of the superior temporal gyrus is occupied by the primary and secondary speech areas. The medial surface shows C-shaped corpus callosum, cingulate gyrus, medial frontal gyrus, cuneus, precuneus, cingulate sulcus and paracentral lobule. The orbital part of the inferior surface shows H-shaped orbital sulcus, olfactory sulcus, and olfactory gyrus. Broca’s motor speech area is present in the dominant hemisphere at the inferior frontal gyrus. Wernicke’s speech area is present in supramarginal and angular gyri. The cerebral hemisphere is mainly supplied by anterior, middle, and posterior cerebral arteries. Understanding the anatomy of the cerebral cortex is critical to recognize the site of lesion in cerebral ischemia.</p> Pradip Chauhan, MBBS, MS, CRM Ashish Rathawa, MBBS, MS Kinjal Jethwa, MBBS, MS Simmi Mehra, MBBS, MS Copyright (c) 2021 Pradip Chauhan, MBBS, MS, CRM , Ashish Rathawa, MBBS, MS , Kinjal Jethwa, MBBS, MS, Simmi Mehra, MBBS, MS https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 1 16 10.36255/exonpublications.cerebralischemia.2021.cerebralcortex The Anatomy of the Hippocampus https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-hippocampus <p><strong>ABSTRACT</strong></p> <p>The hippocampal formation is responsible for memory processing, learning, spatial navigation, and emotions. It includes the indusium griseum, longitudinal striae, gyrus fasciolaris, hippocampus proper (cornu ammonis, dentate gyrus, and subiculum) and part of the uncus. The hippocampus has the archipallial cortex and is formed by the infoldings of the dentate gyrus, cornu ammonis and subiculum. The dentate gyrus is a narrow crenated strip of grey matter. The dentate gyrus consists of three layers, from the outside in: the molecular layer, granular layer, and polymorphic layer.&nbsp; The granular neurons receive input from the parahippocampal gyrus (entorhinal cortex) via the perforant pathway. The granular neurons send mossy fibers to the apical dendrites of pyramidal cells present in the cornu ammonis. The axons of hippocampal pyramidal cells form a sheet of white fibers known as the alveus which continues as fimbria and fornix. The fornix projects into the septal area. From the septal area few fibers synapse into the cingulate gyrus which returns to the hippocampus. The neuronal intrinsic circuit, known as the Papez circuit of the hippocampus, plays a crucial role in the memory processing.</p> Pradip Chauhan, MBBS, MS, CRM Kinjal Jethwa, MBBS, MS Ashish Rathawa, MBBS, MS Girish Chauhan, BDS, MDS Simmi Mehra, MBBS, MS Copyright (c) 2021 Pradip Chauhan, MBBS, MS, CRM, Kinjal Jethwa, MBBS, MS , Ashish Rathawa, MBBS, MS, Girish Chauhan, BDS, MDS, Simmi Mehra, MBBS, MS https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 17 30 10.36255/exonpublications.cerebralischemia.2021.hippocampus Genes Associated with Alzheimer's Disease in Post-Ischemic Brain Neurodegeneration https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-genes <p><strong>ABSTRACT</strong></p> <p>Recent studies have highlighted the role of focal or total ischemia in the development of post-ischemic brain neurodegeneration. However, despite extensive research, the exact mechanism(s) by which ischemia contributes to brain neurodegeneration remains unclear. Therefore, understanding the mechanisms of post-ischemic neurodegeneration of the brain may allow us to develop effective therapies for the prevention and treatment of neurodegenerative diseases. This chapter summarizes the latest research into post-ischemic signaling associated with the development of post-ischemic brain neurodegeneration with Alzheimer's disease-type neuropathology and dementia. We focus mainly on the genes associated with Alzheimer's disease, which play an important role in the development of post-ischemic brain neurodegeneration. Also, the potential role of ischemic factors as new therapeutic targets and prognostic markers in patients with neurodegenerative diseases such as Alzheimer's disease is discussed.</p> Ryszard Pluta, MD, PHD Marzena Ułamek-Kozioł, MD, PHD Copyright (c) 2021 Ryszard Pluta, MD, PHD, Marzena Ułamek-Kozioł, MD, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 31 44 10.36255/exonpublications.cerebralischemia.2021.genes Hypoxic-Ischemic Brain Injury after Perinatal Asphyxia as a Possible Factor in the Pathology of Alzheimer's Disease https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-perinatal-asphyxia <p><strong>ABSTRACT</strong></p> <p>Perinatal asphyxia is a common pathological condition occurring worldwide in approximately 4 million newborns annually. The result of this phenomenon is multi-organ damage and the development of chronic hypoxic encephalopathy. It is currently believed that an episode of cerebral hypoxia/ischemia may be one of the major factors responsible for the development of Alzheimer's disease-type dementia and/or Alzheimer's disease. It cannot be ruled out that hypoxia in the perinatal period may be a trigger factor for the development of Alzheimer's disease in adulthood. The data from scientific research indicate a possible relationship between hypoxia in the earliest stages of life and the occurrence of long lasting genetic and biochemical changes leading to the development of neurodegeneration in Alzheimer’s disease-type.</p> Agata Tarkowska, MD, PHD Copyright (c) 2021 Agata Tarkowska, MD, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 45 59 10.36255/exonpublications.cerebralischemia.2021.perinatalasphyxia Ischemic Brain Injury in Hyperhomocysteinemia https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-hyperhomocysteinemia <p>ABSTRACT</p> <p>Homocysteine is an intermediate product of methionine metabolism. Hyperhomocysteinemia can be caused by high intake of methionine, deficiency of vitamin B<sub>12</sub>, folate, or both. Hyperhomocysteinemia causes cardio- and cerebrovascular diseases, including ischemic stroke. Hyperhomocysteinemia-induced oxidative stress, inflammation, and endoplasmic reticulum stress play an important role in the pathogenesis of several neurodegenerative diseases. Pyramidal neurons of the hippocampus are sensitive to prolonged levels of homocysteine due to the absence of metabolization by transsulfuration as well as by folate- or B<sub>12</sub>- dependent remethylation. This chapter highlights the role of hyperhomocysteinemia in neurodegenerative changes following cerebral ischemia. An overview of how hyperhomocysteinemia by itself, or in combination with ischemia-reperfusion injury, exacerbates neurodegeneration is presented. The role of hyperhomocysteinemia in amyloid deposition and hyperphosphorylation of tau protein in the brain, along with plasma metabolic alterations in cerebral ischemia-reperfusion injury is reviewed. Prevention of hyperhomocysteinemia may have therapeutic implications in cerebral ischemic stroke and deserves investigation.&nbsp;</p> Jan Lehotsky, PHD, DSC Maria Kovalska, PHD Eva Baranovicova, PHD Petra Hnilicova, PHD Dagmar Kalenska, PHD Peter Kaplan, PHD Copyright (c) 2021 Jan Lehotsky, PHD, DSC, Maria Kovalska, PHD , Eva Baranovicova, PHD , Petra Hnilicova, PHD , Dagmar Kalenska, PHD , Peter Kaplan, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 61 72 10.36255/exonpublications.cerebralischemia.2021.hyperhomocysteinemia Exosomes in Post-Ischemic Brain https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-exosomes <p><strong>ABSTRACT</strong></p> <p>Ischemic stroke is a destructive vascular disease that carries the risk of high mortality, disability, and eventually the development of full-blown dementia. Despite the continuous development of new prognostic methods, the prediction of ischemic sequelae and early and late prognosis of stroke is still much easier said than to apply in practice. Cell-to-cell communication between neuronal, glial, and vascular cells are essential for normal functioning of the brain, and in cerebral ischemia, this communication is interrupted. New research has demonstrated the important role of exosomes in cell-to-cell communication via microRNA transfer, playing an integral role in multicellular crosstalk. Following a stroke, harmful and/or beneficial microRNAs are released into the circulation, significantly affecting the severity and prognosis of a stroke. This chapter provides an overview of the current literature on the possible harmful and beneficial roles of cargo derived from exosomes in ischemic stroke. A snapshot of experimental evidence for the role of exosome-derived microRNAs in ischemic stroke followed by clinical studies exploring the diagnostic and prognostic potential of exosomes in stroke patients are presented. Finally, the promises and pitfalls along with future directions are discussed.</p> Ryszard Pluta, MD, PHD Mirosław Jabłoński, MD, PHD Copyright (c) 2021 Mirosław Jabłoński, MD, PHD, Ryszard Pluta, MD, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 73 85 10.36255/exonpublications.cerebralischemia.2021.exosomes Neuroinflammation in Post-Ischemic Brain https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-neuroinflammation <p><strong>ABSTRACT</strong></p> <p>Acute neuroinflammation occurring immediately after cerebral ischemia lasts for a few days. Cytokines and chemokines promote the migration of neutrophils and macrophages to the site of inflammation in the brain. Neuroinflammation lasting 2-6 weeks is known as subacute neuroinflammation, while chronic post-ischemic inflammation lasts for months or years. Macrophages, lymphocytes, and plasma cells predominate in chronic neuroinflammation, in contrast to neutrophils that predominate in acute neuroinflammation. In addition to their harmful impact on the ischemic brain, inflammatory mediators may also exert beneficial effects in stroke recovery. The role of secondary inflammatory cells in the pathophysiology of brain ischemia are still less understood. Late post-ischemic neuroinflammation leads to secondary damage of neuronal cells. In this chapter, the role of leukocytes, T cells, T regs, B cells, neutrophils, macrophages, microglia, astrocytes, cytokines, and transcription factors in the post-ischemic brain are discussed.&nbsp; Post-ischemic thrombo-inflammation and the role of platelets, recently considered as a part of the innate immune system, are also addressed. The current pharmacotherapy and future strategies for the treatment of neuroinflammation in post-ischemic brain as well as the limitations of translation between preclinical and clinical studies are presented.</p> Katarina Živančević, MPHARM Darko Lović, MPHARM Pavle R. Andjus, PHD Lidija Radenovic, PHD Copyright (c) 2021 Katarina Živančević, MSC, Darko Lović, MSC , Pavle R. Andjus, PHD , Lidija Radenovic https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 87 109 10.36255/exonpublications.cerebralischemia.2021.neuroinflammation Neurovascular Reactivity in Tissue Scarring Following Cerebral Ischemia https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-neurovascular-reactivity <p><strong>ABSTRACT</strong></p> <p>Tissue scarring upon cerebral ischemia entails a cascade of multifaceted cellular and molecular mechanisms that govern the remodeling of the neurovascular unit, which integrates neuronal, glial, and vascular functions.&nbsp; The process encompasses inflammation, glial reactivity, vascular reactivity, and neuronal remodeling. In this chapter we cover three major aspects involved in tissue scarring after cerebral ischemia. First, we outline the primary cellular mechanisms underlying glial scar formation, emphasizing on the interactions between astrocytes, microglia, and mural cells, including pericytes and fibroblasts at the injury core and perilesional areas. Next, we address the key routes of extracellular matrix deposition by reactive and fibrogenic cells, including proteoglycans, tenascins, fibronectin, and collagen. Finally, we discuss the promises and challenges of manipulating tissue scarring as a strategy to promote brain structural remodeling and neurological recovery.</p> Daniel Manrique-Castano, PHD Ayman ElAli, PHD Copyright (c) 2021 Daniel Manrique-Castano, PHD, Ayman ElAli, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 111 129 10.36255/exonpublications.cerebralischemia.2021.neurovascularreactivity The Role of Cathepsin B in Ischemia-Reperfusion Injury After Stroke https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-cathepsin <p><strong>ABSTRACT</strong></p> <p>Cathepsins are endolysosomal proteases that can be categorized into different types based on their structures and active-site amino acid residue, including cysteine (cathepsins B, C, F, H, K, L, O, S, V, W, and X), serine (cathepsins A and G), and aspartic (cathepsins D and E). Cathepsins can regulate diverse cellular activities such as the processing and presentation of antigens, the processing and activation of hormones, apoptosis, aging, and autophagy. Recently, cathepsin B has gained attention for its role in various neurological diseases including ischemic stroke, Alzheimer’s disease, Parkinson’s disease, and traumatic brain injury. This chapter mainly focuses on the role of cathepsin B in brain ischemia reperfusion injury in animal models of stroke.</p> Bhakta Prasad Gaire, PHD Lalita Subedi, PHD Hironori Teramoto, BSC Bingren Hu, PHD Copyright (c) 2021 Bhakta Prasad Gaire, PHD, Lalita Subedi, PHD, Hironori Teramoto, BSC, Bingren Hu, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 131 147 10.36255/exonpublications.cerebralischemia.2021.cathepsin The Role of Curcumin in Post-Ischemic Brain https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-curcumin <p><strong>ABSRACT</strong></p> <p>Progressive accumulation of misfolded amyloid and tau protein in intracellular and extracellular spaces is the most crucial etiopathological feature of brain ischemia, synaptic damage, or neural communication impairment. Clinical data suggest that dietary intake of curcumin enhances neurogenesis and offers neuroprotection. Curcumin is a natural polyphenolic compound with diverse and attractive biological properties. It may prevent aging-associated changes in cellular proteins, such as β-amyloid peptide and tau protein, that lead to protein insolubility and aggregation after ischemic brain damage. Therefore, curcumin seems to be a promising supplementary agent against neurodegeneration development after brain ischemia. The aim of this chapter is to highlight our current understanding of the neuroprotective role of curcumin in cerebral ischemia-reperfusion injury. The limitations and adverse events of curcumin are also presented.</p> Marta Rusek, PHD Stanislaw Czuczwar, MD, PHD Copyright (c) 2021 Marta Rusek, PHD, Stanislaw Czuczwar, MD, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 149 164 10.36255/exonpublications.cerebralischemia.2021.curcumin Treating Cerebral Ischemia: Novel Therapeutic Strategies from Experimental Stroke Research https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-therapy <p><strong>ABSTRACT</strong></p> <p>Although systemic thrombolysis and endovascular treatment have revolutionized modern stroke treatment, the majority of patients do not qualify for either treatment paradigm. Hence, novel adjuvant therapeutic strategies are required. This chapter provides an overview of our current understanding of novel therapeutic strategies in preclinical stroke models. The chapter is organized in three major parts to cover the acute, subacute, and chronic phases of ischemic stroke. The potential of various pharmacological agents, stem cells, microRNAs, and extracellular vesicles as therapeutic avenues along with the progress and challenges are discussed.</p> Xuan Zheng, MSC Matteo Haupt, BSC Mathias Bähr, MD Lars Tatenhorst, PHD Thorsten R. Doeppner, MD, MSC Copyright (c) 2021 Xuan Zheng, MSC , Matteo Haupt, BSC , Mathias Bähr, MD , Lars Tatenhorst, PHD , Thorsten R. Doeppner, MD, MSC https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 165 185 10.36255/exonpublications.cerebralischemia.2021.therapy Community-Based Rehabilitation After Brain Infarction in Japan: From the Acute Phase to Home https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-rehabilitation <p><strong>ABSTRACT</strong></p> <p>Cerebral infarction is one of the most common cerebrovascular diseases and can result in severe residual functional disabilities that permanently affect patients’ activities of daily living and quality of life. Rehabilitation plays a significant role in reintegrating these people into society and enabling them to return home. Due to the growing aging population in Japan, the financial and societal impacts of cerebrovascular diseases are expected to increase. Here, we review the rehabilitation process in Japan through the acute, recovery, and daily living stages while considering the pathological conditions of patients with cerebral infarction. In particular, we discuss the pathology of cerebral infarction and rehabilitation interventions, the timing and purpose of rehabilitation, the use of walking aids such as canes, braces, and walking-assistive robots, the benefits of providing support and guidance to family members and caregivers, the use of telestroke and telerehabilitation, the services provided by rehabilitation facilities, and recent legal changes in Japan.</p> Shinichiro Maeshima, MD, PHD Aiko Osawa, MD, PHD Copyright (c) 2021 Shinichiro Maeshima, MD, PHD, Aiko Osawa, MD, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 187 200 10.36255/exonpublications.cerebralischemia.2021.rehabilitation Understanding Social Risk Variation Across Reintegration of Post-Ischemic Stroke Patients https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-reintegration <p><strong>ABSTRACT</strong></p> <p>The quality of life of post-ischemic stroke patients during reintegration is affected by a range of factors, including the risk of insufficient social and family support, as well as socio-economic status. A patient who is unable to access needed social support, such as home health care or a day center, is at a greater risk of poorer quality of life during reintegration. Consequently, the key goals of post-stroke reintegration are to improve patient outcomes across these factors, to inform reintegration decisions, as well as design personalized interventions for patients with social risk. This chapter presents a case-study of 240 patients of the Catalonia region of Spain that uses data visualization techniques (known as Sankey diagrams) to provide insight into changes in quality of life risk factors such as gender, and stroke severity, during reintegration. As supported by the case-study, social risk is a complex and multifactorial phenomenon that can vary significantly for an individual over the course of stroke rehabilitation and reintegration.</p> Katryna Cisek, PHD Thi Nguyet Que Nguyen, PHD Alejandro Garcia-Rudolph, PHD Joan Saurí, PHD John D. Kelleher, PHD Copyright (c) 2021 Katryna Cisek, PHD, Thi Nguyet Que Nguyen, PHD, Alejandro Garcia-Rudolph, PHD , Joan Saurí, PHD, John D. Kelleher, PHD https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 201 219 10.36255/exonpublications.cerebralischemia.2021.reintegration Index https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-index Index Copyright (c) 2021 Exon Publications https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 221 224 10.36255/exonpublications.cerebralischemia.2021.index About the Editor https://exonpublications.com/index.php/exon/article/view/cerebral-ischemia-editor <p><img src="https://exonpublications.com/public/site/images/bchapter/r.pluta-for-upload.jpg" alt="Ryszard Pluta" width="156" height="201"></p> <p>Professor Ryszard Pluta, MD, PhD, is the head of the Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland. He has held positions at the National Institutes of Health, Bethesda, USA, at the Institute for Basic Research in Developmental Disabilities, Staten Island, USA, and at the Max-Planck Institute for Neurological Research in Cologne, Germany. Professor Pluta was awarded by the Polish Association of Neuropathologists, President of Polish Academy of Sciences, Medical Secretary of Polish Academy of Sciences, Batory’s Foundation in Warsaw, Poland, International Brain Research Organization in Paris, France, and Alzheimer’s Association Chicago, USA. In 2017, Professor Pluta was awarded the Maria Curie-Skłodowska statuette. In New York in 1994 he was the first to propose the ischemic etiology of Alzheimer’s disease, followed by publications in which he presented proteomic and genomic alterations in the ischemic brain that are identical to those in Alzheimer’s disease. In 1998, he was the first to present autoimmunization as a new therapy for Alzheimer’s disease. Professor Pluta has published more than 250 peer-reviewed scientific articles and his current research focuses on developing ischemic model of Alzheimer’s disease. He is listed among the top 2% outstanding scientists in the world.</p> Ryszard Pluta, MD, PhD (Editor) Copyright (c) 2021 https://creativecommons.org/licenses/by-nc/4.0 2021-11-06 2021-11-06 10.36255/exonpublications.cerebralischemia.2021.editor