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Novel therapeutic strategies targeting mitochondria as a gateway in neurodegeneration

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Neural Regeneration Research 2023年第5期18卷 991-995页

作者： Diogo Trigo Jose Joao Vitoria Odete A.B.da Cruz e Silva Neuroscience and Signalling Laboratory Institute of Biomedicine(iBiMED)Department of Medical SciencesUniversity of AveiroAveiroPortugal

In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that have a variety of functions in ensuring cellular health and homeostasis. The plethora of mitochondrial functionalities confers them an intrinsic susceptibility to internal and external stressors(such as mutation accumulation or environmental toxins), particularly so in long-lived postmitotic cells such as neurons. Thus, it is reasonable to postulate an involvement of mitochondria in aging-associated neurological disorders, notably neurodegenerative pathologies including Alzheimer’s disease and Parkinson’s disease. On the other hand, biological effects resulting from neurodegeneration can in turn affect mitochondrial health and function, promoting a feedback loop further contributing to the progression of neuronal dysfunction and cellular death. This review examines state-of-the-art knowledge, focus on current research exploring mitochondrial health as a contributing factor to neuroregeneration, and the development of therapeutic approaches aimed at restoring mitochondrial homeostasis in a pathological setting.

关键词： Alzheimer’s disease axon energy homeostasis glymphatic system mitochondria mitostasis neurodegeneration neuroregeneration Parkinson’s disease therapeutical strategies

axon regeneration induced by environmental enrichment-epigenetic mechanisms

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Neural Regeneration Research 2020年第1期15卷 10-15页

作者： Bor Luen Tang Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Graduate School for Integrative Sciences and Engineering National University of Singapore

Environmental enrichment is known to be beneficial for cognitive improvement.In many animal models of neurological disorders and brain injury,EE has also demonstrated neuroprotective benefits in neurodegenerative diseases and in improving recovery after stroke or traumatic brain injury.The exact underlying mechanism for these phenomena has been unclear.Recent findings have now indicated that neuronal activity elicited by environmental enrichment induces Ca2+influx in dorsal root ganglion neurons results in lasting enhancement of CREB-binding protein-mediated histone acetylation.This,in turn,increases the expression of pro-regeneration genes and promotes axonal regeneration.This mechanism associated with neuronal activity elicited by environmental enrichment-mediated pathway is one of several epigenetic mechanisms which modulate axon regeneration upon injury that has recently come to light.The other prominent mechanisms,albeit not yet directly associated with environmental enrichment,include DNA methylation/demethylation and N6-methyladenosine modification of transcripts.In this brief review,I highlight recent work that has shed light on the epigenetic basis of environmental enrichment-based axon regeneration,and discuss the mechanism and pathways involved.I further speculate on the implications of the findings,in conjunction with the other epigenetic mechanisms,that could be harness to promote axon regeneration upon injury.

关键词： axon regeneration CREB-binding protein DNA methylation/demethylation dorsal root ganglion DRG neurons environmental enrichment epigenetics histone acetylation mechanistic target of rapamycin mTOR phosphatase and tensin homologue PTEN

Potential physiological and pathological roles for axonal ryanodine receptors

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Neural Regeneration Research 2023年第4期18卷 756-759页

作者： David P.Stirling Kentucky Spinal Cord Injury Research Center and Departments of Neurological Surgery Anatomical Sciences and NeurobiologyMicrobiology and ImmunologyUniversity of LouisvilleSchool of MedicineLouisvilleKYUSA

Clinical disability following trauma or disease to the spinal cord often involves the loss of vital white matter elements including axons and glia.Although excessive Cais an established driver of axonal degeneration,therapeutically targeting externally sourced Cato date has had limited success in both basic and clinical studies.Contributing factors that may underlie this limited success include the complexity of the many potential sources of Caentry and the discovery that axons also contain substantial amounts of stored Cathat if inappropriately released could contribute to axonal demise.axonal Castorage is largely accomplished by the axoplasmic reticulum that is part of a continuous network of the endoplasmic reticulum that provides a major sink and source of intracellular Cafrom the tips of dendrites to axonal terminals.This“neuron-within-a-neuron”is positioned to rapidly respond to diverse external and internal stimuli by amplifying cytosolic Calevels and generating short and long distance regenerative Cawaves through Cainduced Carelease.This review provides a glimpse into the molecular machinery that has been implicated in regulating ryanodine receptor mediated Carelease in axons and how dysregulation and/or overstimulation of these internodal axonal signaling nanocomplexes may directly contribute to Ca-dependent axonal demise.Neuronal ryanodine receptors expressed in dendrites,soma,and axonal terminals have been implicated in synaptic transmission and synaptic plasticity,but a physiological role for internodal localized ryanodine receptors remains largely obscure.Plausible physiological roles for internodal ryanodine receptors and such an elaborate internodal binary membrane signaling network in axons will also be discussed.

关键词： axomyelinic synapse axon axoplasmic reticulum calcium ryanodine receptor secondary axonal degeneration spinal cord injury voltage-gated calcium channel white matter injury

Neuroaxonal and cellular damage/protection by prostanoid receptor ligands,fatty acid derivatives and associated enzyme inhibitors

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Neural Regeneration Research 2023年第1期18卷 5-17页

作者： Najam A.Sharif Department of Pharmaceutical Sciences College of Pharmacy and Health SciencesTexas Southern UniversityHoustonTXUSA Department of Pharmacology and Neuroscience University of North Texas Health Sciences CenterFort WorthTXUSA Department of Pharmacy Sciences School of Pharmacy and Health ProfessionsCreighton UniversityOmahaNEUSA Singapore Eye Research Institute(SERI) SingaporeSingapore Duke-NUS Medical School SingaporeSingapore Department of Surgery&Cancer Imperial College of Science and TechnologySt.Mary’s CampusLondonUK Global Alliances and External Research Ophthalmology Innovation CenterSanten Inc USAEmeryvilleCAUSA

Cellular and mitochondrial membrane phospholipids provide the substrate for synthesis and release of prostaglandins in response to certain chemical,mechanical,noxious and other stimuli.Prostaglandin D_(2),prostaglandin E_(2),prostaglandin F_(2)α,prostaglandin I_(2)and thromboxane-A_(2)interact with five major receptors(and their sub-types)to elicit specific downstream cellular and tissue actions.In general,prostaglandins have been associated with pain,inflammation,and edema when they are present at high local concentrations and involved on a chronic basis.However,in acute settings,certain endogenous and exogenous prostaglandins have beneficial effects ranging from mediating muscle contraction/relaxation,providing cellular protection,regulating sleep,and enhancing blood flow,to lowering intraocular pressure to prevent the development of glaucoma,a blinding disease.Several classes of prostaglandins are implicated(or are considered beneficial)in certain central nervous system dysfunctions(e.g.,Alzheimer’s,Parkinson’s,and Huntington’s diseases;amyotrophic lateral sclerosis and multiple sclerosis;stroke,traumatic brain injuries and pain)and in ocular disorders(e.g.,ocular hypertension and glaucoma;allergy and inflammation;edematous retinal disorders).This review endeavors to address the physiological/pathological roles of prostaglandins in the central nervous system and ocular function in health and disease,and provides insights towards the therapeutic utility of some prostaglandin agonists and antagonists,polyunsaturated fatty acids,and cyclooxygenase inhibitors.

关键词： AL-8810 axon brain central nervous system cyclooxygenase inhibitors neuron neuroprotection ocular polyunsaturated fatty acids prostaglandins

TC10 as an essential molecule in axon regeneration through membrane supply and microtubule stabilization

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Neural Regeneration Research 2022年第1期17卷 87-88页

作者： Takeshi Nakamura Shingo Koinuma Division of Cell Signaling Research Institute for Biomedical SciencesTokyo University of ScienceNodaJapan

Mammalian central nervous system(CNS)neurons lose axon regenerative ability as they mature.This failure to regenerate shows a clear contrast to a remarkable potential of axon growth during embryonic development and after an injury in the peripheral nervous system(PNS)(Hilton and Bradke,2017).The absence of regeneration in the mature CNS neurons is caused by an inhibitory influence of the environment of the injured axons and the deficit of intrinsic factors that enable regeneration in the PNS(He and Jin,2016).

关键词： stabilization enable axon

Reduced graphene oxide-embedded nerve conduits loaded with bone marrow mesenchymal stem cell-derived extracellular vesicles promote peripheral nerve regeneration

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Neural Regeneration Research 2023年第1期18卷 200-206页

作者： Wei Zhang Xing-Xing Fang Qi-Cheng Li Wei Pi Na Han Department of Orthopedics and Trauma Peking University People’s HospitalBeijingChina National Center for Trauma Medicine BeijingChina Central Laboratory Peking University People’s HospitalBeijingChina

We previously combined reduced graphene oxide(rGO)with gelatin-methacryloyl(GelMA)and polycaprolactone(PCL)to create an rGO-GelMA-PCL nerve conduit and found that the conductivity and biocompatibility were improved.However,the rGO-GelMA-PCL nerve conduits differed greatly from autologous nerve transplants in their ability to promote the regeneration of injured peripheral nerves and axonal sprouting.Extracellular vesicles derived from bone marrow mesenchymal stem cells(BMSCs)can be loaded into rGO-GelMA-PCL nerve conduits for repair of rat sciatic nerve injury because they can promote angiogenesis at the injured site.In this study,12 weeks after surgery,sciatic nerve function was measured by electrophysiology and sciatic nerve function index,and myelin sheath and axon regeneration were observed by electron microscopy,immunohistochemistry,and immunofluorescence.The regeneration of microvessel was observed by immunofluorescence.Our results showed that rGO-GelMA-PCL nerve conduits loaded with BMSC-derived extracellular vesicles were superior to rGO-GelMA-PCL conduits alone in their ability to increase the number of newly formed vessels and axonal sprouts at the injury site as well as the recovery of neurological function.These findings indicate that rGO-GelMA-PCL nerve conduits loaded with BMSC-derived extracellular vesicles can promote peripheral nerve regeneration and neurological function recovery,and provide a new direction for the curation of peripheral nerve defect in the clinic.

关键词： angiogenesis axon bone mesenchymal stem cell extracellular vesicles hybrid nanofibers myelin sheath nerve conduit neurological function peripheral nerve injury reduced graphene oxide

Biomimetic chitosan scaffolds with long-term controlled release of nerve growth factor repairs 20-mm-long sciatic nerve defects in rats

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Neural Regeneration Research 2022年第5期17卷 1146-1155页

作者： Fa-Dong Liu Hong-Mei Duan Fei Hao Wen Zhao Yu-Dan Gao Peng Hao Zhao-Yang Yang Xiao-Guang Li Beijing Key Laboratory for Biomaterials and Neural Regeneration School of Biological Science and Medical EngineeringBeihang UniversityBeijingChina Department of Neurobiology Capital Medical UniversityBeijingChina Beijing International Cooperation Bases for Science and Technology on Biomaterials and Neural Regeneration Beijing Advanced Innovation Center for Biomedical EngineeringBeihang UniversityBeijingChina

Although autogenous nerve transplantation is the gold standard for treating peripheral nerve defects of considerable length,it still has some shortcomings,such as insufficient donors and secondary injury.Composite chitosan scaffolds loaded with controlled release of nerve growth factor can promote neuronal survival and axonal regeneration after short-segment sciatic nerve defects.However,the effects on extended nerve defects remain poorly understood.In this study,we used chitosan scaffolds loaded with nerve growth factor for 8 weeks to repair long-segment(20 mm)sciatic nerve defects in adult rats.The results showed that treatment markedly promoted the recovery of motor and sensory functions.The regenerated sciatic nerve not only reconnected with neurons but neural circuits with the central nervous system were also reconstructed.In addition,the regenerated sciatic nerve reconnected the motor endplate with the target muscle.Therefore,this novel biomimetic scaffold can promote the regeneration of extended sciatic nerve defects and reconstruct functional circuits.This provides a promising method for the clinical treatment of extended peripheral nerve injury.This study was approved by the Animal Ethics Committee of Capital Medical University,China(approval No.AEEI-2017-033)on March 21,2017.

关键词： axon chitosan functional recovery myelin sheath nerve growth factor peripheral nerve injury pseudorabies virus regeneration scaffold sciatic nerve

Overcoming axon regeneration failure and psychopathology:how may gabapentinoids help boost CNS repair?

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Neural Regeneration Research 2023年第8期18卷 1703-1704页

作者： Haven I.Rodocker Andrea Tedeschi Department of Neuroscience Wexner Medical CenterThe Ohio State UniversityColumbusOHUSA Chronic Brain Injury Program The Ohio State UniversityColumbusOHUSA

Spinal cord injury (SCI) at the cervical level compromises the function of both upper and lower extremities, thereby impeding an individual’s ability to complete daily tasks required for independent living and profoundly affecting the overall quality of life among individuals afflicted by SCI and their families. Recovery of spinal cord functions may be attained by promoting the sprouting of non-injured axons and/or the regeneration of damaged axons.

关键词： thereby boost axon

Acetyl-11-keto-beta-boswellic acid promotes sciatic nerve repair after injury: molecular mechanism

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Neural Regeneration Research 2022年第12期17卷 2778-2784页

作者： Yao Wang Zong-Liang Xiong Xiang-Lin Ma Chong Zhou Mo-Han Huo Xiao-Wen Jiang Wen-Hui Yu Department of Veterinary Medicine Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina College of Life Sciences Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina Key Laboratory of Heilongjiang Education Department for Common Animal Disease Prevention and Treatment Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina Institute of Chinese Veterinary Medicine Northeast Agricultural UniversityHarbinHeilongjiang ProvinceChina

Previous studies showed that acetyl-11-keto-beta-boswellic acid(AKBA),the active ingredient in the natural Chinese medicine Boswellia,can stimulate sciatic nerve injury repair via promoting Schwann cell proliferation.However,the underlying molecular mechanism remains poorly understood.In this study,we performed genomic sequencing in a rat model of sciatic nerve crush injury after gastric AKBA administration for 30 days.We found that the phagosome pathway was related to AKBA treatment,and brain-derived neurotrophic factor expression in the neurotrophic factor signaling pathway was also highly up-regulated.We further investigated gene and protein expression changes in the phagosome pathway and neurotrophic factor signaling pathway.Myeloperoxidase expression in the phagosome pathway was markedly decreased,and brain-derived neurotrophic factor,nerve growth factor,and nerve growth factor receptor expression levels in the neurotrophic factor signaling pathway were greatly increased.Additionally,expression levels of the inflammatory factors CD68,interleukin-1β,pro-interleukin-1β,and tumor necrosis factor-αwere also decreased.Myelin basic protein-andβ3-tubulin-positive expression as well as the axon diameter-to-total nerve diameter ratio in the injured sciatic nerve were also increased.These findings suggest that,at the molecular level,AKBA can increase neurotrophic factor expression through inhibiting myeloperoxidase expression and reducing inflammatory reactions,which could promote myelin sheath and axon regeneration in the injured sciatic nerve.

关键词： AKBA axon genomics inflammatory injury and repair myelin sheath myeloperoxidase neurotrophic factor peripheral nerve phagosome pathway regeneration Sprague-Dawley rat