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| 1 | Role of axon resealing in retrograde neuronal death and regeneration after spinal cord injury显示文摘Spinal cord injury leads to persistent behavioral deficits because mammalian central nervous system axons fail to regenerate. A neuron's response to axon injury results from a complex interplay of neuron-intrinsic and environmental factors. The contribution of axotomy to the death of neurons in spinal cord injury is controversial because very remote axotomy is unlikely to result in neuronal death, whereas death of neurons near an injury may reflect environmental factors such as ischemia and inflammation. In lampreys, axotomy due to spinal cord injury results in delayed apoptosis of spinal-projecting neurons in the brain, beyond the extent of these environmental factors. This retrograde apoptosis correlates with delayed resealing of the axon, and can be reversed by inducing rapid membrane resealing with polyethylene glycol. Studies in mammals also suggest that polyethylene glycol may be neuroprotective, although the mechanism(s) remain unclear. This review examines the early, mechanical, responses to axon injury in both mammals and lampreys, and the potential of polyethylene glycol to reduce injury-induced pathology. Identifying the mechanisms underlying a neuron's response to axotomy will potentially reveal new therapeutic targets to enhance regeneration and functional recovery in humans with spinal cord injury. | William Rodemer Michael E.Selzer | 2019 | Neural Regeneration Research2019，14，3： | 4 |
| 2 | Oligodendrocyte pathology in fetal alcohol spectrum disorders显示文摘The pathology of fetal alcohol syndrome and the less severe fetal alcohol spectrum disorders includes brain dysmyelination.Recent studies have shed light on the molecular mechanisms underlying these white matter abnormalities.Rodent models of fetal alcohol syndrome and human studies have shown suppressed oligodendrocyte differentiation and apoptosis of oligodendrocyte precursor cells.Ethanol exposure led to reduced expression of myelin basic protein and delayed myelin basic protein expression in rat and mouse models of fetal alcohol syndrome and in human histopathological specimens.Several studies have reported increased expression of many chemokines in dysmyelinating disorders in central nervous system,including multiple sclerosis and fetal alcohol syndrome.Acute ethanol exposure reduced levels of the neuroprotective insulin-like growth factor-1 in fetal and maternal sheep and in human fetal brain tissues,while ethanol increased the expression of tumor necrosis factor α in mouse and human neurons.White matter lesions have been induced in the developing sheep brain by alcohol exposure in early gestation.Rat fetal alcohol syndrome models have shown reduced axon diameters,with thinner myelin sheaths,as well as reduced numbers of oligodendrocytes,which were also morphologically aberrant oligodendrocytes.Expressions of markers for mature myelination,including myelin basic protein,also were reduced.The accumulating knowledge concerning the mechanisms of ethanol-induced dysmyelination could lead to the development of strategies to prevent dysmyelination in children exposed to ethanol during fetal development.Future studies using fetal oligodendrocyte-and oligodendrocyte precursor cell-derived exosomes isolated from the mother's blood may identify biomarkers for fetal alcohol syndrome and even implicate epigenetic changes in early development that affect oligodendrocyte precursor cell and oligodendrocyte function in adulthood.By combining various imaging modalities with molecular studies,it may be possible to determine which fetuses are at risk and to intervene therapeutically early in the pregnancy. | Nune Darbinian Michael E.Selzer | 2022 | Neural Regeneration Research2022，17，3： | 1 |
| 3 | Inhibition of central axon regeneration: perspective from chondroitin sulfate proteoglycans in lamprey spinal cord injury显示文摘Background:Failure of axon regeneration after spinal cord injury(SCI)underlies the paralysis that so profoundly affects patients’quality of life.Many factors are involved in the regeneration failure.Chondroitin sulfate proteoglycans(CSPGs),normal constituents of the perineuronal nets in central nervous system(CNS),are secreted at the injury site and initially were thought to act as a purely physical barrier.In the past decade,the receptor-like protein tyrosine phosphatases,protein tyrosine phosphatase sigma(PTPσ),and leukocyte common antigen-related phosphatase(LAR),have been identified as transmembrane receptors for CSPGs.The two receptors for myelin-associated growth inhibitors,Nogo receptors 1 and 3(NgR1 and NgR3)also have been found to bind with CSPGs(Sharma et al.,2012).These findings suggest that CSPGs inhibit regeneration by interacting with these receptors,initiating downstream inhibitory signaling(Figure 1). | Jianli Hu Li-Qing Jin Michael E.Selzer | 2022 | Neural Regeneration Research2022，17，9： | 1 |
| 4 | Heterogeneity in the regenerative abilities of central nervous system axons within species: why do some neurons regenerate better than others?显示文摘Some neurons,especially in mammalian peripheral nervous system or in lower vertebrate or in vertebrate central nervous system(CNS)regenerate after axotomy,while most mammalian CNS neurons fail to regenerate.There is an emerging consensus that neurons have different intrinsic regenerative capabilities,which theoretically could be manipulated therapeutically to improve regeneration.Population-based comparisons between'good regenerating'and'bad regenerating'neurons in the CNS and peripheral nervous system of most vertebrates yield results that are inconclusive or difficult to interpret.At least in part,this reflects the great diversity of cells in the mammalian CNS.Using mammalian nervous system imposes several methodical limitations.First,the small sizes and large numbers of neurons in the CNS make it very difficult to distinguish regenerating neurons from non-regenerating ones.Second,the lack of identifiable neurons makes it impossible to correlate biochemical changes in a neuron with axonal damage of the same neuron,and therefore,to dissect the molecular mechanisms of regeneration on the level of single neurons.This review will survey the reported responses to axon injury and the determinants of axon regeneration,emphasizing non-mammalian model organisms,which are often under-utilized,but in which the data are especially easy to interpret. | William Rodemer Jianli Hu Michael E.Selzer Michael I.Shifman | 2020 | Neural Regeneration Research2020，15，6： | 0 |
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