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      Cerebral ischemia and neuroregeneration

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          Abstract

          Cerebral ischemia is one of the leading causes of morbidity and mortality worldwide. Although stroke (a form of cerebral ischemia)-related costs are expected to reach 240.67 billion dollars by 2030, options for treatment against cerebral ischemia/stroke are limited. All therapies except anti-thrombolytics ( i.e., tissue plasminogen activator) and hypothermia have failed to reduce neuronal injury, neurological deficits, and mortality rates following cerebral ischemia, which suggests that development of novel therapies against stroke/cerebral ischemia are urgently needed. Here, we discuss the possible mechanism(s) underlying cerebral ischemia-induced brain injury, as well as current and future novel therapies ( i.e., growth factors, nicotinamide adenine dinucleotide, melatonin, resveratrol, protein kinase C isozymes, pifithrin, hypothermia, fatty acids, sympathoplegic drugs, and stem cells) as it relates to cerebral ischemia.

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          Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration.

          Liya Qin, Xuefei Wu, Michelle L. Block … (2007)
          Inflammation is implicated in the progressive nature of neurodegenerative diseases, such as Parkinson's disease, but the mechanisms are poorly understood. A single systemic lipopolysaccharide (LPS, 5 mg/kg, i.p.) or tumor necrosis factor alpha (TNFalpha, 0.25 mg/kg, i.p.) injection was administered in adult wild-type mice and in mice lacking TNFalpha receptors (TNF R1/R2(-/-)) to discern the mechanisms of inflammation transfer from the periphery to the brain and the neurodegenerative consequences. Systemic LPS administration resulted in rapid brain TNFalpha increase that remained elevated for 10 months, while peripheral TNFalpha (serum and liver) had subsided by 9 h (serum) and 1 week (liver). Systemic TNFalpha and LPS administration activated microglia and increased expression of brain pro-inflammatory factors (i.e., TNFalpha, MCP-1, IL-1beta, and NF-kappaB p65) in wild-type mice, but not in TNF R1/R2(-/-) mice. Further, LPS reduced the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra (SN) by 23% at 7-months post-treatment, which progressed to 47% at 10 months. Together, these data demonstrate that through TNFalpha, peripheral inflammation in adult animals can: (1) activate brain microglia to produce chronically elevated pro-inflammatory factors; (2) induce delayed and progressive loss of DA neurons in the SN. These findings provide valuable insight into the potential pathogenesis and self-propelling nature of Parkinson's disease. (c) 2007 Wiley-Liss, Inc.
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            Neuronal replacement from endogenous precursors in the adult brain after stroke.

            Andreas Arvidsson, Tove Collin, Deniz Kirik … (2002)
            In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans.
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              Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention.

              Alok Kumar, David J Loane (2012)
              Traumatic brain injury (TBI) remains one of the leading causes of mortality and morbidity worldwide, yet despite extensive efforts to develop neuroprotective therapies for this devastating disorder there have been no successful outcomes in human clinical trials to date. Following the primary mechanical insult TBI results in delayed secondary injury events due to neurochemical, metabolic and cellular changes that account for many of the neurological deficits observed after TBI. The development of secondary injury represents a window of opportunity for therapeutic intervention to prevent progressive tissue damage and loss of function after injury. To establish effective neuroprotective treatments for TBI it is essential to fully understand the complex cellular and molecular events that contribute to secondary injury. Neuroinflammation is well established as a key secondary injury mechanism after TBI, and it has been long considered to contribute to the damage sustained following brain injury. However, experimental and clinical research indicates that neuroinflammation after TBI can have both detrimental and beneficial effects, and these likely differ in the acute and delayed phases after injury. The key to developing future anti-inflammatory based neuroprotective treatments for TBI is to minimize the detrimental and neurotoxic effects of neuroinflammation while promoting the beneficial and neurotrophic effects, thereby creating optimal conditions for regeneration and repair after injury. This review outlines how post-traumatic neuroinflammation contributes to secondary injury after TBI, and discusses the complex and varied responses of the primary innate immune cells of the brain, microglia, to injury. In addition, emerging experimental anti-inflammatory and multipotential drug treatment strategies for TBI are discussed, as well as some of the challenges faced by the research community to translate promising neuroprotective drug treatments to the clinic. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Regen Res
                Journal ID (iso-abbrev): Neural Regen Res
                Journal ID (publisher-id): NRR
                Title: Neural Regeneration Research
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 1673-5374
                ISSN (Electronic): 1876-7958
                Publication date (Print): March 2018
                Volume: 13
                Issue: 3
                Pages: 373-385
                Affiliations
                [1 ]Department of Neurology, Louisiana State University Health Science Center, Shreveport, LA, USA
                [2 ]Center for Brain Health, Louisiana State University Health Science Center, Shreveport, LA, USA
                [3 ]Department of Cellular Biology and Anatomy, Louisiana State University Health Science Center, Shreveport, LA, USA
                [4 ]Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan, China
                [5 ]Cardiovascular and Metabolomics Research Center, Hualien Tzu Chi Hospital, Hualien, Taiwan, China
                Author notes
                [* ] Correspondence to: Hung Wen Lin, hlin2@ 123456lsuhsc.edu .
                [#]

                These authors contributed equally to this work.

                Author contributions: RHCL, MHHL: drafted manuscript, revised manuscript critically for important intellectual content, and final approval. CYCW, ACS, HEP, THH: drafted manuscript and final approval. AM, and HWL: revised manuscript critically for important intellectual content and final approval.

                Author information
                http://orcid.org/0000-0003-1010-5423
                Article
                Publisher ID: NRR-13-373
                DOI: 10.4103/1673-5374.228711
                PMC ID: 5900490
                PubMed ID: 29623912
                SO-VID: 7ea84e26-918e-4a5d-828a-d7e968e2df2e
                Copyright © Copyright: © Neural Regeneration Research
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                Date accepted : 01 February 2018
                Categories
                Subject: Invited Review

                Keywords: cerebral ischemia,melatonin,resveratrol,protein kinase c,pifithrin-α,fatty acids,sympathetic nervous system,neuromodulation therapy,traditional chinese therapies,stem cell
                Data availability:
                Keywords: cerebral ischemia, melatonin, resveratrol, protein kinase c, pifithrin-α, fatty acids, sympathetic nervous system, neuromodulation therapy, traditional chinese therapies, stem cell

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