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Neural Regeneration Research 2022年第1期17卷 91-92页

作者： Rayudu Gopalakrishna Charlotte Lin Mark S.Kindy William J.Mack Department of Integrative Anatomical Sciences Keck School of MedicineUniversity of Southern CaliforniaLos AngelesCAUSA Department of Neurological Surgery Keck School of MedicineUniversity of Southern CaliforniaLos AngelesCAUSA Department of Pharmaceutical Sciences College of PharmacyUniversity of South FloridaTampaFLUSA

Currently,there are no clinically proven drugs for recovery from stroke and other neuronal injuries such as traumatic brain injury and spinal cord injury.Recovery therapy requires axonal regeneration,which is inhibited by diverse axonal growth inhibitors,such as Nogo-A,myelin-associated glycoprotein(MAG),oligodendrocyte myelin glycoprotein(OMgp),and chondroitin sulfate proteoglycans(CSPGs)(Chaudhry and Filbin,2007;Carmichael,2010;Schwab and Strittmatter,2014).

关键词： axonal injuries inhibited

Barriers to axonal regeneration after spinal cord injury:a current perspective

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Neural Regeneration Research 2022年第1期17卷 85-86页

作者： Jacek M.Kwiecien Department of Pathology and Molecular Medicine Faculty of Health SciencesMcMaster UniversityHamiltonOntarioCanada

Regeneration of long axons after the spinal cord injury(SCI)will benefit patients with extensive traumatic damage to the white matter pathways who experience intolerable,permanent,neurologic deficits even after neuroprotective treatment with anti-inflammatory agents(Kwiecien,2021a).This short paper attempts to synthetize pathologic mechanisms or barriers involved in inhibition of axonal regeneration in the SCI and provides suggestions of therapeutic interventions enabling this regeneration in animal models.

关键词： protective axonal injury

Non-cell autonomous role of astrocytes in axonal degeneration of cortical projection neurons in hereditary spastic paraplegias

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Neural Regeneration Research 2022年第6期17卷 1265-1266页

作者： Xue-Jun Li Department of Biomedical Sciences University of Illinois College of Medicine RockfordRockfordILUSA Department of Bioengineering University of Illinois at ChicagoChicagoILUSA

Impai red axonal deve lopment and degeneration underlie many debilitating diseases,including hereditary spastic paraplegia(HSP).HSPs are a heterogeneous group of neurogenetic disorders characterized by axonopathy of cortical motor neurons(Fink,2006;Blackstone et al.,2010).The axonal degeneration of these cortical projection neurons(PNs)in HSP patients disrupts the signals from brain to spinal motor neurons,leading to muscle weakness and spasticity.Since the discovery of the first HSP gene(SPAST)in 1999,over 80 distinct genetic loci associated with HSP have been identified.How the mutations of these divergent genes specifically result in axonal degeneration of cortical PNs remains largely unclear,which contributes to the lack of effective treatment to ameliorate,stop,or reverse axonal defects in HSPs.

关键词： degeneration axonal projection

Approaches to quantify axonal morphology for the analysis of axonal degeneration

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Neural Regeneration Research 2023年第2期18卷 309-310页

作者： Alex Palumbo Marietta Zille Department of Neurobiology Harvard Medical School Department of Cancer Biology Dana-Farber Cancer InstituteBostonMAUSA Department of Pharmaceutical Sciences Division of Pharmacology and ToxicologyUniversity of ViennaViennaAustria

Morphological hallmarks of axonal degeneration(AxD):Axons transmit signals from one neuron to another and a re crucial for the proper communication in the nervous system.Therefore,the disintegration of axons,a process... 详细信息

关键词： degeneration axonal Morphological

Molecular mechanisms of lesion-induced axonal sprouting in the corticofugal projection:the role of glial cells

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Neural Regeneration Research 2023年第6期18卷 1259-1260页

作者： Leechung Chang Nobuhiko Yamamoto Laboratory of Cellular and Molecular Neurobiology Graduate School of Frontier BiosciencesOsaka UniversitySuitaOsakaJapan

After injury of the central nervous system(CNS),neuronal circuits are known to remodel for functional recovery.In general,there are two strategies for the remodeling:axonal regeneration and sprouting(Figure 1A).axonal regeneration is re-growth of injured neurons themselves,but axons hardly regenerate in the adult mammalian CNS(Silver and Miller,2004).On the other hand,axonal sprouting is new growth from intact or spared neurons to the denervated target by forming axon collaterals,compensating for damaged circuits.This process is a more effective way for circuit remodeling,as it does not necessarily require long axonal elongation.

关键词： axonal projection Figure

Inhibiting endogenous tissue plasminogen activator enhanced neuronal apoptosis and axonal injury after traumatic brain injury

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Neural Regeneration Research 2020年第4期15卷 667-675页

作者： Jun-Jie Zhao Zun-Wei Liu Bo Wang Ting-Qin Huang Dan Guo Yong-Lin Zhao Jin-Ning Song Department of Neurosurgery the First Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Institute of Organ Transplantation the First Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Department of Renal Transplantation Nephropathy Hospitalthe First Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Department of Neurosurgery the Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina Department of Science and Technology Xi’an Medical UniversityXi’anShaanxi ProvinceChina Department of Oncology the Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’anShaanxi ProvinceChina

Tissue plasminogen activator is usually used for the treatment of acute ischemic stroke,but the role of endogenous tissue plasminogen activator in traumatic brain injury has been rarely reported.A rat model of traumatic brain injury was established by weight-drop method.The tissue plasminogen activator inhibitor neuroserpin(5μL,0.25 mg/mL)was injected into the lateral ventricle.Neurological function was assessed by neurological severity score.Neuronal and axonal injuries were assessed by hematoxylin-eosin staining and Bielschowsky silver staining.Protein level of endogenous tissue plasminogen activator was analyzed by western blot assay.Apoptotic marker cleaved caspase-3,neuronal marker neurofilament light chain,astrocyte marker glial fibrillary acidic protein and microglial marker Iba-1 were analyzed by immunohistochemical staining.Apoptotic cell types were detected by immunofluorescence double labeling.Apoptotic cells in the damaged cortex were detected by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling staining.Degenerating neurons in the damaged cortex were detected by Fluoro-Jade B staining.Expression of tissue plasminogen activator was increased at 6 hours,and peaked at 3 days after traumatic brain injury.Neuronal apoptosis and axonal injury were detected after traumatic brain injury.Moreover,neuroserpin enhanced neuronal apoptosis,neuronal injury and axonal injury,and activated microglia and astrocytes.Neuroserpin further deteriorated neurobehavioral function in rats with traumatic brain injury.Our findings confirm that inhibition of endogenous tissue plasminogen activator aggravates neuronal apoptosis and axonal injury after traumatic brain injury,and activates microglia and astrocytes.This study was approved by the Biomedical Ethics Committee of Animal Experiments of Shaanxi Province of China in June 2015.

关键词： apoptosis astrocytes axonal injury inflammation microglia nerve regeneration neural regeneration neuronal injury neurons neuroserpin tissue plasminogen activator traumatic brain injury

Rescue axonal defects by targeting mitochondrial dynamics in hereditary spastic paraplegias

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Neural Regeneration Research 2019年第4期14卷 574-577页

作者： Yongchao Mou Xue-Jun Li Department of Biomedical Sciences University of Illinois College of Medicine Rockford Department of Bioengineering University of Illinois at Chicago

Impaired axonal development and degeneration underlie debilitating neurodegenerative diseases including hereditary spastic paraplegia, a large group of inherited diseases. Hereditary spastic paraplegia is caused by retrograde degeneration of the long corticospinal tract axons, leading to progressive spasticity and weakness of leg and hip muscles. There are over 70 subtypes with various underlying pathophysiological processes, such as defective vesicular trafficking, lipid metabolism, organelle shaping, axonal transport, and mitochondrial dysfunction. Although hereditary spastic paraplegia consists of various subtypes with different pathological characteristics, defects in mitochondrial morphology and function emerge as one of the common cellular themes in hereditary spastic paraplegia. Mitochondrial morphology and function are remodeled by mitochondrial dynamics regulated by several key fission and fusion mediators. However, the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia remains largely unknown. Recently, studies reported perturbed mitochondrial morphology in hereditary spastic paraplegia neurons. Moreover, downregulation of mitochondrial fission regulator dynamin-related protein 1, both pharmacologically and genetically, could rescue axonal outgrowth defects in hereditary spastic paraplegia neurons, providing a potential therapeutic target for treating these hereditary spastic paraplegia. This mini-review will describe the regulation of mitochondrial fission/fusion, the link between mitochondrial dynamics and axonal defects, and the recent progress on the role of mitochondrial dynamics in axonal defects of hereditary spastic paraplegia.

关键词： hereditary spastic paraplegia axonal degeneration mitochondrial dynamics fission fusion dynamin-related protein 1 mitochondrial dysfunction induced pluripotent stem cells

A lead role for a“secondary”axonal injury response

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Neural Regeneration Research 2025年第2期20卷 469-470页

作者： Melissa A.Rudy Trent A.Watkins Division of Neuroimmunology and Glial Biology Department of NeurologyUniversity of California at San FranciscoSan FranciscoCAUSA Development Disease Modelsand Therapeutics Graduate ProgramBaylor College of MedicineHoustonTXUSA

Stress signaling following axon injury stimulates a transcriptional program for regeneration that might be exploited to promote central nervous system repair.However,this stress response drives neuronal apoptosis in non-regenerative environments.This duality presents a quandary for the development of therapeutic interventions:manipulating stress signaling to enhance recovery of damaged neurons risks accelerating neurodegeneration or restricting regenerative potential.This dichotomy is well illustrated by the fates of retinal ganglion cells(RGCs)following optic nerve crush.In this central nervous system injury model,disruption of a stress-activated MAP kinase(MAPK)cascade blocks the extensive apoptosis of RGCs that occurs in wild-type mice(Watkins et al.,2013;Welsbie et al.,2017).

关键词： injury axonal stress

Compartmentalized necroptosis activation in excitotoxicityinduced axonal degeneration: a novel mechanism implicated in neurodegenerative disease pathology

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Neural Regeneration Research 2019年第8期14卷 1385-1386页

作者： Macarena S. Arrazola Felipe A. Court Center for Integrative Biology Faculty of Sciences Universidad Mayor de Chile Santiago CnileFONDAP Center for Geroscience Brain Health and Metabolism Santiago Chile Buck Institute for Research on Ageing Novato San Francisco CA USA

Excitotoxicity and neuronal cell death: Glutamate is the main excitatory neurotransmitter of the central nervous system and functionally involved in most brain activities, including brain development, synaptic plasticity, learning and memory. Exc让atory synaptic transmission is primarily mediated by ligana-gated ion channels, including a-amino-3-hydroxy-5-methylisoxazoIe-4-propionic acid (AMPA), N-methyl-D-aspartate (NMDA) and kainate receptors. Activation of glutamate receptors, particularly NMDA receptors, usually leads to calcium influx, whicn can act as a second messenger for several processes to mediate synaptic activity and brain function. Nevertheless, excessive release of glutamate neurotransmitter may produce intracellular calcium overload, leading to a cascade of events mediating cytoskeleton damage accompanied w让h reactive oxygen species (ROS) generation, mitochondrial dysfunction and ultimately neuronal cell death. These toxic effects of glutamate are known as excitotoxicity. Neuronal excitotoxicity has been linked to several acute and chronic brain diseases, such as stroke/ischemia, epilepsy and a range of neurodegenerative disorders, including Alzheimer's disease (AD), Huntingtons disease, amyotrophic lateral sclerosis (ALS) and Parkinsons disease (PD), contributing to the neuronal lost in different brain regions. Unfortunately, treating nervous system disorders with general glutamate receptor blockers has been associated with undesirable side effects, becoming increasingly necessary to unravel downstream effectors in the excitotoxicity-dependent cell death pathway in order to develop novel therapeutic strategies.

关键词： Compartmentalized necroptosis activation excitotoxicityinduced axonal neurodegenerative disease

Two novel mutations in theGAN gene causing giant axonal neuropathy

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World Journal of Pediatrics 2018年第3期14卷 298-304页

作者： Monica Irad Normendez-Martínez Lucero Monterde-Cruz Roberto Martínez Magdalena Marquez-Harper Nayelli Esquitin-Garduno Margarita Valdes-Flores Leonora Casas-Avila Valeria Ponce de Leon-Suarez Viktor Javier Romero-Díaz Alberto Hidalgo-Bravo Medical Specialties Hospital Boulevard Milenio 130San Carlos la Roncha37660 LeonGuanajuatoMexico Department of Gene tics National Institute of R ehabilitationAvenue Mexico-Xochimilco 28914389 Me xico CityMexico Department ofHis tology School ofMedicineAutonomous University oft heS tate ofN uevo LeonMonterreyMexico

Background Giant axonal neuropathy (GAN) is a rare neurodegenerative disease transmitted in an autosomal recessive mode. This disorder presents motor and sensitive symptoms with an onset in early childhood. Progressive neurodegeneration makes the patients wheelchair dependent by the end of the second decade of life. Affected individuals do not survive beyond the third decade of life. Molecular analysis has identified mutations in the gene GAN in patients with this disorder. This gene produces a protein called gigaxonin which is presumably involved in protein degradation via the ubiquitin-proteasome system. However, the underlying molecular mechanism is not clearly understood yet. Methods Here we present the fi rst patient from Mexico with clinical data suggesting GAN. Sequencing of the GAN gene was carried out. Changes in the nucleotide sequence were investigated for their possible impact on protein function and structure using the publicly available prediction tools PolyPhen-2 and PANTHER. Results The patient is a compound heterozygous carrying two novel mutations in the GAN gene. The sequence analy-sis revealed two missense mutations in the Kelch repeats domain. In one allele, a C>T transition was found in exon 9 at the nucleotide position 55393 (g.55393C>T). In the other allele, a transversion G>T in exon 11 at the nucleotide position 67471 (g.67471G>T) was observed. Both of the bioinformatic tools predicted that these amino acid substitutions would have a negative impact on gigaxonin's function. Conclusion This work provides useful information for health professionals and expands the spectrum of disease-causing mutations in the GAN gene and it is the first documented case in Mexican population.

关键词： GAN Genetics Giant axonal neuropathy Incapacity Neurodegenerative