Log in

Relevant bibliographies by topics / Nervous system – Degeneration / Journal articles

Journal articles on the topic 'Nervous system – Degeneration'

To see the other types of publications on this topic, follow the link: Nervous system – Degeneration.

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Nervous system – Degeneration.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Longstreth, George F., and Frederick D. Walker. "Megaesophagus and Hereditary Nervous System Degeneration." Journal of Clinical Gastroenterology 19, no. 2 (September 1994): 125–27. http://dx.doi.org/10.1097/00004836-199409000-00010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Avramut, M., and C. Achim. "Immunophilins in Nervous System Degeneration and Regeneration." Current Topics in Medicinal Chemistry 3, no. 12 (August 1, 2003): 1376–82. http://dx.doi.org/10.2174/1568026033451871.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Love, S. "DEGENERATION AND REGENERATION IN THE NERVOUS SYSTEM." Brain 126, no. 4 (April 1, 2003): 1009–11. http://dx.doi.org/10.1093/brain/awg078.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Tsimkhes, I. L. "Trauma and Peripheral Nervous System. Brun (Schweiz, med. Wochenschr. 1931, 11)." Kazan medical journal 29, no. 4 (November 19, 2021): 359. http://dx.doi.org/10.17816/kazmj88621.

Full text

Abstract:

Brun (Schweiz, med. Wochenschr. 1931, 11) distinguishes neuritis ascendens associated with the area of the skin on which the infected wound was located, and organic symptoms are subsequently often replaced by psychogenic fixation of pain. The atrophies that occur from inactivity differ from degenerative atrophies in the absence of a degeneration reaction and a uniform spread to the veto muscle.

APA, Harvard, Vancouver, ISO, and other styles

5

Mietto, Bruno Siqueira, Klauss Mostacada, and Ana Maria Blanco Martinez. "Neurotrauma and Inflammation: CNS and PNS Responses." Mediators of Inflammation 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/251204.

Full text

Abstract:

Traumatic injury to the central nervous system (CNS) or the peripheral nervous system (PNS) triggers a cascade of events which culminate in a robust inflammatory reaction. The role played by inflammation in the course of degeneration and regeneration is not completely elucidated. While, in peripheral nerves, the inflammatory response is assumed to be essential for normal progression of Wallerian degeneration and regeneration, CNS trauma inflammation is often associated with poor recovery. In this review, we discuss key mechanisms that trigger the inflammatory reaction after nervous system trauma, emphasizing how inflammations in both CNS and PNS differ from each other, in terms of magnitude, cell types involved, and effector molecules. Knowledge of the precise mechanisms that elicit and maintain inflammation after CNS and PNS tissue trauma and their effect on axon degeneration and regeneration is crucial for the identification of possible pharmacological drugs that can positively affect the tissue regenerative capacity.

APA, Harvard, Vancouver, ISO, and other styles

6

Lo, Eng H. "Degeneration and repair in central nervous system disease." Nature Medicine 16, no. 11 (September 21, 2010): 1205–9. http://dx.doi.org/10.1038/nm.2226.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Lexell, Jan. "Evidence for Nervous System Degeneration with Advancing Age." Journal of Nutrition 127, no. 5 (May 1, 1997): 1011S—1013S. http://dx.doi.org/10.1093/jn/127.5.1011s.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Leech, R. W., D. L. Feeback, M. S. Burton, and E. C. Ramsav. "SPONGY DEGENERATION OF THE NERVOUS SYSTEM IN SITATUNGA." Journal of Neuropathology and Experimental Neurology 45, no. 3 (May 1986): 344. http://dx.doi.org/10.1097/00005072-198605000-00092.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Subramanyam, Sarvepalli B., Aparna Tipirneni, Nazih Youssef, Generoso G. Gascon, and Pinar T. Ozand. "Biochemical Heterogeneity of Infantile Central Nervous System Spongy Degeneration." Journal of Child Neurology 7, no. 1_suppl (April 1992): S22—S25. http://dx.doi.org/10.1177/08830738920070010411.

Full text

Abstract:

Aspartoacylase, the enzyme whose activity is deficient in infantile central nervous system spongy degeneration (Canavan-Van Bogaert-Bertrand disease), is detected as an approximately 59-kD protein in the Sephadex G-200 filtration of normal fibroblast extracts. The enzyme activity in homogenates of fibroblasts is protected by leupeptin, a protease inhibitor. In the absence of leupeptin, 90% of aspartoacylase activity is lost. In some patients with infantile spongy degeneration, no activity (less than 2%) can be detected. In some other patients with residual activity in fibroblasts, two separate peaks of enzyme are eluted with molecular weight corresponding to approximately 59 and 19 kD. Aspartoacylase activity in this latter group is protected to the same extent by the presence of leupeptin. However, the elution of two peaks is independent of the presence of leupeptin. This study indicates biochemical heterogeneity in the pathogenesis of infantile spongy degeneration. (J Child Neurol 1992;7(Suppl):S22-S25.)

APA, Harvard, Vancouver, ISO, and other styles

10

Jortner, Bernard S. "Common Structural Lesions of the Peripheral Nervous System." Toxicologic Pathology 48, no. 1 (February 5, 2019): 96–104. http://dx.doi.org/10.1177/0192623319826068.

Full text

Abstract:

This review illustrates common lesions of peripheral nerve myelinated fibers that occur in toxic neuropathy. These distinctive structural changes help to define the site of toxicant activity and thus predict the course of neurotoxic disease and recovery. Neuronopathy is the condition where the primary injury is directed to the neuronal cell body giving rise to a peripheral nerve axon. Axonopathy occurs when the axon is the primary target, and myelinopathy develops where the Schwann cell and/or myelin sheath is the primary target; these conditions can be discriminated early during the course of nerve fiber degeneration, but reciprocal influences between axon and myelin result in degeneration of both structures late in the disease.

APA, Harvard, Vancouver, ISO, and other styles

11

Compston, Alastair. "Remyelination of the central nervous system." Multiple Sclerosis Journal 1, no. 6 (June 1996): 388–92. http://dx.doi.org/10.1177/135245859600100622.

Full text

Abstract:

The three typical stages in the clinical course of multiple sclerosis (relapse, persistent disability and progression) can be explained on the basis of inflammation, demyelination and failure of repair leading to axon degeneration and astrocytosis. Strategies ore being evaluated for limiting the inflammatory process using immunological treatments and these may have unexpected dividends in promoting endogenous remyelination. Increasing knowledge on glial lineages and axon-glial interactions needed for stable myelination also offer the prospect for enhancing remyelination through growth factor therapy and cell implantation.

APA, Harvard, Vancouver, ISO, and other styles

12

Aguayo, Albert J. "Symposium 5: Degeneration and Regeneration in the Nervous System." Brain Pathology 4, no. 4 (September 1994): 303–4. http://dx.doi.org/10.1111/j.1750-3639.1994.tb00909.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Cartelli, Daniele, Guido Cavaletti, Giuseppe Lauria, and Cristina Meregalli. "Ubiquitin Proteasome System and Microtubules Are Master Regulators of Central and Peripheral Nervous System Axon Degeneration." Cells 11, no. 8 (April 15, 2022): 1358. http://dx.doi.org/10.3390/cells11081358.

Full text

Abstract:

Axonal degeneration is an active process that differs from neuronal death, and it is the hallmark of many disorders affecting the central and peripheral nervous system. Starting from the analyses of Wallerian degeneration, the simplest experimental model, here we describe how the long projecting neuronal populations affected in Parkinson’s disease and chemotherapy-induced peripheral neuropathies share commonalities in the mechanisms and molecular players driving the earliest phase of axon degeneration. Indeed, both dopaminergic and sensory neurons are particularly susceptible to alterations of microtubules and axonal transport as well as to dysfunctions of the ubiquitin proteasome system and protein quality control. Finally, we report an updated review on current knowledge of key molecules able to modulate these targets, blocking the on-going axonal degeneration and inducing neuronal regeneration. These molecules might represent good candidates for disease-modifying treatment, which might expand the window of intervention improving patients’ quality of life.

APA, Harvard, Vancouver, ISO, and other styles

14

Furutani-Seiki, M., Y. J. Jiang, M. Brand, C. P. Heisenberg, C. Houart, D. Beuchle, F. J. van Eeden, et al. "Neural degeneration mutants in the zebrafish, Danio rerio." Development 123, no. 1 (December 1, 1996): 229–39. http://dx.doi.org/10.1242/dev.123.1.229.

Full text

Abstract:

Forty zebrafish mutants with localized or general neural degeneration are described. The onset and duration of degeneration and the distribution of ectopically dying cells are specific characteristics of each mutant. Mutants are classified into four groups by these parameters. Class I: late focal neural degeneration mutants. These 18 mutants have restricted cell death mainly in the tectum and the dorsal hindbrain after 36 hours. The degeneration does not spread and disappears at later stages of development. Class II: early focal neural degeneration mutants. Ten mutants in this class exhibit transient restricted degeneration affecting mainly the diencephalon, the hindbrain and the spinal cord at 20 hours. The midbrain is less affected. The degeneration shifts to the dorsal diencephalon and the tectum at 36 hours. Class III: late spreading neural degeneration mutants. The 8 mutants in this class display a degeneration that is first seen in the tectum and subsequently spreads throughout the nervous system from 36 hours on. Class IV: early general neural degeneration mutants. This class of four mutants already shows overall cell degeneration in the nervous system at the 15-somite stage. Three of the class I mutants show a change in the pattern of gene expression in the anlage of a brain structure prior to the onset of degeneration. These results suggest that focal cell death may be a useful clue for the detection of early patterning defects of the vertebrate nervous system in regions devoid of visible landmarks.

APA, Harvard, Vancouver, ISO, and other styles

15

Rodriguez, Michael, and Wolfgang Driever. "Mutations resulting in transient and localized degeneration in the developing zebrafish brain." Biochemistry and Cell Biology 75, no. 5 (October 1, 1997): 579–600. http://dx.doi.org/10.1139/o97-089.

Full text

Abstract:

In a large-scale mutagenesis screen in the zebrafish, Danio rerio, we have identified a heterogeneous group of 30 recessive, embryonic lethal mutations characterized by degeneration in the developing central nervous system that is either transient or initially localized to one area of the brain. Transient degeneration is defined as abnormal cell death occurring during a restricted period of development. Following degeneration, the affected structures do not appear to regenerate. In each case degeneration is identified after somitogenesis is complete and is not associated with visually identified patterning defects. These 30 mutations, forming 21 complementation groups, have been classified into four phenotypic groups: group 1, transient degeneration (13 mutations); group 2, spreading degeneration, early onset, in which degeneration is initially confined to the optic tectum but subsequently spreads to other areas of the central nervous system (7 mutations); group 3, late-onset degeneration, initially identified after 4 days (6 mutations); and group 4, degeneration with abnormal pigmentation (4 mutations). Although apoptotic cells are seen in the retina and tectum of all mutants, the distribution, temporal progression, and severity of degeneration vary between mutations. Several mutations also show pleiotropic effects, with degeneration involving extraneural structures including the pharyngeal arches and pectoral fins. We discuss some of the pathways important for cell survival in the nervous system and suggest that these mutations will provide entry points for identifying genes that affect the survival of restricted neural populations.

APA, Harvard, Vancouver, ISO, and other styles

16

Minn, Yang-Ki, Seung-Min Kim, Se-Hoon Kim, Ki-Han Kwon, and Il-Nam Sunwoo. "Sequential Involvement of the Nervous System in Subacute Combined Degeneration." Yonsei Medical Journal 53, no. 2 (2012): 276. http://dx.doi.org/10.3349/ymj.2012.53.2.276.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Lehky, T., P. Sackstein, D. Tamura, M. Quezado, T. Wu, S. G. Khan, N. J. Patronas, et al. "150 Peripheral nervous system degeneration in patients with xeroderma pigmentosum." Journal of Investigative Dermatology 141, no. 5 (May 2021): S27. http://dx.doi.org/10.1016/j.jid.2021.02.170.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

YAMASAKI, HIROSHI, MASANOBU GORYO, TAKASHI UMEMURA, KOICHI OTA, and TOKUMARO FUKUI. "Spongy Degeneration of the Central Nervous System in a Calf." Journal of the Japan Veterinary Medical Association 41, no. 7 (1988): 514–16. http://dx.doi.org/10.12935/jvma1951.41.514.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Tseng, Kuang-Wen, Mei-Lin Peng, Yang-Cheng Wen, Kang-Jen Liu, and Chung-Liang Chien. "Neuronal degeneration in autonomic nervous system of Dystonia musculorum mice." Journal of Biomedical Science 18, no. 1 (2011): 9. http://dx.doi.org/10.1186/1423-0127-18-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Castaño, Angélica, Michael D. Bell, and V. Hugh Perry. "Unusual aspects of inflammation in the nervous system: Wallerian degeneration." Neurobiology of Aging 17, no. 5 (September 1996): 745–51. http://dx.doi.org/10.1016/0197-4580(96)00105-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Zhou, Zijian, Dake Qi, Quan Gan, Fang Wang, Bengang Qin, Jiachun Li, Honggang Wang, and Dong Wang. "Studies on the Regulatory Roles and Related Mechanisms of lncRNAs in the Nervous System." Oxidative Medicine and Cellular Longevity 2021 (March 13, 2021): 1–12. http://dx.doi.org/10.1155/2021/6657944.

Full text

Abstract:

Long noncoding RNAs (lncRNAs) have attracted extensive attention due to their regulatory role in various cellular processes. Emerging studies have indicated that lncRNAs are expressed to varying degrees after the growth and development of the nervous system as well as injury and degeneration, thus affecting various physiological processes of the nervous system. In this review, we have compiled various reported lncRNAs related to the growth and development of central and peripheral nerves and pathophysiology (including advanced nerve centers, spinal cord, and peripheral nervous system) and explained how these lncRNAs play regulatory roles through their interactions with target-coding genes. We believe that a full understanding of the regulatory function of lncRNAs in the nervous system will contribute to understand the molecular mechanism of changes after nerve injury and will contribute to discover new diagnostic markers and therapeutic targets for nerve injury diseases.

APA, Harvard, Vancouver, ISO, and other styles

22

Yin, Xinghua, Rena C. Baek, Daniel A. Kirschner, Alan Peterson, Yasuhisa Fujii, Klaus-Armin Nave, Wendy B. Macklin, and Bruce D. Trapp. "Evolution of a neuroprotective function of central nervous system myelin." Journal of Cell Biology 172, no. 3 (January 30, 2006): 469–78. http://dx.doi.org/10.1083/jcb.200509174.

Full text

Abstract:

The central nervous system (CNS) of terrestrial vertebrates underwent a prominent molecular change when a tetraspan membrane protein, myelin proteolipid protein (PLP), replaced the type I integral membrane protein, P0, as the major protein of myelin. To investigate possible reasons for this molecular switch, we genetically engineered mice to express P0 instead of PLP in CNS myelin. In the absence of PLP, the ancestral P0 provided a periodicity to mouse compact CNS myelin that was identical to mouse PNS myelin, where P0 is the major structural protein today. The PLP–P0 shift resulted in reduced myelin internode length, degeneration of myelinated axons, severe neurological disability, and a 50% reduction in lifespan. Mice with equal amounts of P0 and PLP in CNS myelin had a normal lifespan and no axonal degeneration. These data support the hypothesis that the P0–PLP shift during vertebrate evolution provided a vital neuroprotective function to myelin-forming CNS glia.

APA, Harvard, Vancouver, ISO, and other styles

23

Becker, Laren, Linh Nguyen, Jaspreet Gill, Subhash Kulkarni, Pankaj Jay Pasricha, and Aida Habtezion. "Age-dependent shift in macrophage polarisation causes inflammation-mediated degeneration of enteric nervous system." Gut 67, no. 5 (February 21, 2017): 827–36. http://dx.doi.org/10.1136/gutjnl-2016-312940.

Full text

Abstract:

ObjectiveThe enteric nervous system (ENS) undergoes neuronal loss and degenerative changes with age. The cause of this neurodegeneration is poorly understood. Muscularis macrophages residing in close proximity to enteric ganglia maintain neuromuscular function via direct crosstalk with enteric neurons and have been implicated in the pathogenesis of GI motility disorders like gastroparesis and postoperative ileus. The aim of this study was to assess whether ageing causes alterations in macrophage phenotype that contributes to age-related degeneration of the ENS.DesignLongitudinal muscle and myenteric plexus from small intestine of young, mid-aged and old mice were dissected and prepared for whole mount immunostaining, flow cytometry, Luminex immunoassays, western blot analysis, enteric neural stem cell (ENSC) isolation or conditioned media. Bone marrow derived macrophages were prepared and polarised to classic (M1) or alternative (M2) activation states. Markers for macrophage phenotype were measured using quantitative RT-PCR.ResultsAgeing causes a shift in macrophage polarisation from anti-inflammatory ‘M2’ to proinflammatory ‘M1’ that is associated with a rise in cytokines and immune cells in the ENS. This phenotypic shift is associated with a neural response to inflammatory signals, increase in apoptosis and loss of enteric neurons and ENSCs, and delayed intestinal transit. An age-dependent decrease in expression of the transcription factor FoxO3, a known longevity gene, contributes to the loss of anti-inflammatory behaviour in macrophages of old mice, and FoxO3-deficient mice demonstrate signs of premature ageing of the ENS.ConclusionsA shift by macrophages towards a proinflammatory phenotype with ageing causes inflammation-mediated degeneration of the ENS.

APA, Harvard, Vancouver, ISO, and other styles

24

Butt, Mark T. "Sampling and Evaluating the Peripheral Nervous System." Toxicologic Pathology 48, no. 1 (July 25, 2019): 10–18. http://dx.doi.org/10.1177/0192623319862540.

Full text

Abstract:

Many preclinical investigations limit the evaluation of the peripheral nervous system (PNS) to paraffin-embedded sections/hematoxylin and eosin–stained sections of the sciatic nerve. This limitation ignores several key mechanisms of toxicity and anatomic differences that may interfere with an accurate assessment of test article effects on the neurons/neurites peripheral to the brain and spinal cord. Ganglion neurons may be exposed to higher concentrations of the test article as compared to neurons in the brain or spinal cord due to differences in capillary permeability. Many peripheral neuropathies are length-dependent, meaning distal nerves may show morphological changes before they are evident in the mid-sciatic nerve. Paraffin-embedded nerves are not optimal to assess myelin changes, notably those leading to demyelination. Differentiating between axonal or myelin degeneration may not be possible from the examination of paraffin-embedded sections. A sampling strategy more consistent with known mechanisms of toxicity, atraumatic harvest of tissues, optimized fixation, and the use of resin and paraffin-embedded sections will greatly enhance the pathologist’s ability to observe and characterize effects in the PNS.

APA, Harvard, Vancouver, ISO, and other styles

25

Sato, Yuichiro, and Kurt Benirschke. "Amnion Degeneration over Fetal Placental Surface Vessels Possibly Resulting from Focal Hypoxia: A Case Report." Pediatric and Developmental Pathology 9, no. 3 (May 2006): 225–28. http://dx.doi.org/10.2350/06-01-0011.1.

Full text

Abstract:

The monoamnionic placenta of this twin gestation had focal amnion necrosis, but this was present only over the fetal surface vessels of one twin; this twin also developed cerebral atrophy. We hypothesize that this degeneration is due to a more severely reduced oxygen tension in its vessels. The placental amnion epithelium may undergo several degenerative processes, including amnion nodosum and changes due to meconium staining. Sonography had disclosed what appeared to be a dividing membrane, but this was not found at birth when monoamnionic twins with entangled cords presented. The amnion degeneration was present only over the large surface fetal vessels of the placenta of that twin who also developed central nervous system degeneration, and macrophage infiltration was confined to the same lesions. Focal hypoxia from entangling cords may have caused this defect.

APA, Harvard, Vancouver, ISO, and other styles

26

Sun, Yue, Qi Wang, Yi Wang, Wenran Ren, Ying Cao, Jiali Li, Xin Zhou, Wei Fu, and Jing Yang. "Sarm1-mediated neurodegeneration within the enteric nervous system protects against local inflammation of the colon." Protein & Cell 12, no. 8 (April 19, 2021): 621–38. http://dx.doi.org/10.1007/s13238-021-00835-w.

Full text

Abstract:

AbstractAxonal degeneration is one of the key features of neurodegenerative disorders. In the canonical view, axonal degeneration destructs neural connections and promotes detrimental disease defects. Here, we assessed the enteric nervous system (ENS) of the mouse, non-human primate, and human by advanced 3D imaging. We observed the profound neurodegeneration of catecholaminergic axons in human colons with ulcerative colitis, and similarly, in mouse colons during acute dextran sulfate sodium-induced colitis. However, we unexpectedly revealed that blockage of such axonal degeneration by the Sarm1 deletion in mice exacerbated the colitis condition. In contrast, pharmacologic ablation or chemogenetic inhibition of catecholaminergic axons suppressed the colon inflammation. We further showed that the catecholaminergic neurotransmitter norepinephrine exerted a pro-inflammatory function by enhancing the expression of IL-17 cytokines. Together, this study demonstrated that Sarm1-mediated neurodegeneration within the ENS mitigated local inflammation of the colon, uncovering a previously-unrecognized beneficial role of axonal degeneration in this disease context.

APA, Harvard, Vancouver, ISO, and other styles

27

Kang, Eugene Yu-Chuan, Pei-Kang Liu, Yao-Tseng Wen, Peter M. J. Quinn, Sarah R. Levi, Nan-Kai Wang, and Rong-Kung Tsai. "Role of Oxidative Stress in Ocular Diseases Associated with Retinal Ganglion Cells Degeneration." Antioxidants 10, no. 12 (December 5, 2021): 1948. http://dx.doi.org/10.3390/antiox10121948.

Full text

Abstract:

Ocular diseases associated with retinal ganglion cell (RGC) degeneration is the most common neurodegenerative disorder that causes irreversible blindness worldwide. It is characterized by visual field defects and progressive optic nerve atrophy. The underlying pathophysiology and mechanisms of RGC degeneration in several ocular diseases remain largely unknown. RGCs are a population of central nervous system neurons, with their soma located in the retina and long axons that extend through the optic nerve to form distal terminals and connections in the brain. Because of this unique cytoarchitecture and highly compartmentalized energy demand, RGCs are highly mitochondrial-dependent for adenosine triphosphate (ATP) production. Recently, oxidative stress and mitochondrial dysfunction have been found to be the principal mechanisms in RGC degeneration as well as in other neurodegenerative disorders. Here, we review the role of oxidative stress in several ocular diseases associated with RGC degenerations, including glaucoma, hereditary optic atrophy, inflammatory optic neuritis, ischemic optic neuropathy, traumatic optic neuropathy, and drug toxicity. We also review experimental approaches using cell and animal models for research on the underlying mechanisms of RGC degeneration. Lastly, we discuss the application of antioxidants as a potential future therapy for the ocular diseases associated with RGC degenerations.

APA, Harvard, Vancouver, ISO, and other styles

28

Galli, Jonathan, and John Greenlee. "Paraneoplastic Diseases of the Central Nervous System." F1000Research 9 (March 6, 2020): 167. http://dx.doi.org/10.12688/f1000research.21309.1.

Full text

Abstract:

Paraneoplastic neurological syndromes are nonmetastatic complications of malignancy secondary to immune-mediated neuronal dysfunction or death. Pathogenesis may occur from cell surface binding of antineuronal antibodies leading to dysfunction of the target protein, or from antibodies binding against intracellular antigens which ultimately leads to cell death. There are several classical neurological paraneoplastic phenotypes including subacute cerebellar degeneration, limbic encephalitis, encephalomyelitis, and dorsal sensory neuropathy. The patient’s clinical presentations may be suggestive to the treating clinician as to the specific underlying paraneoplastic antibody. Specific antibodies often correlate with the specific underlying tumor type, and malignancy screening is essential in all patients with paraneoplastic neurological disease. Prompt initiation of immunotherapy is essential in the treatment of patients with paraneoplastic neurological disease, often more effective in cell surface antibodies in comparison to intracellular antibodies, as is removal of the underlying tumor.

APA, Harvard, Vancouver, ISO, and other styles

29

Cuartas Arias, Jorge Mauricio. "Cognition and inflammation: “the role of cytokines in cognitive performance”." International Journal of Psychological Research 7, no. 2 (July 1, 2014): 8–10. http://dx.doi.org/10.21500/20112084.653.

Full text

Abstract:

The interactions between the immune system and nervous system have been the focus of research in recent years. Perhaps due to the discovery and acknowledgement of the multiple functions that cytokines carry out in the central nervous system (CNS), going from mediators of neuropathologic processes to the degeneration and repair within the CNS.

APA, Harvard, Vancouver, ISO, and other styles

30

Melchor, Jerry, and Sidney Strickland. "Tissue plasminogen activator in central nervous system physiology and pathology." Thrombosis and Haemostasis 93, no. 04 (2005): 655–60. http://dx.doi.org/10.1160/th04-12-0838.

Full text

Abstract:

SummaryAlthough conventionally associated with fibrin clot degradation, recent work has uncovered new functions for the tissue plasminogen activator (tPA)/plasminogen cascade in central nervous system physiology and pathology. This extracellular proteolytic cascade has been shown to have roles in learning and memory, stress, neuronal degeneration, addiction and Alzheimer’s disease. The current review considers the different ways tPA functions in the brain.

APA, Harvard, Vancouver, ISO, and other styles

31

Brisby, Helena. "Pathology and Possible Mechanisms of Nervous System Response to Disc Degeneration." Journal of Bone and Joint Surgery (American) 88, suppl_2 (April 1, 2006): 68. http://dx.doi.org/10.2106/jbjs.e.01282.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

BRISBY, HELENA. "PATHOLOGY AND POSSIBLE MECHANISMS OF NERVOUS SYSTEM RESPONSE TO DISC DEGENERATION." Journal of Bone and Joint Surgery-American Volume 88 (April 2006): 68–71. http://dx.doi.org/10.2106/00004623-200604002-00014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Beirowski, Bogdan, Antal Nógrádi, Elisabetta Babetto, Guillermo Garcia-Alias, and Michael P. Coleman. "Mechanisms of Axonal Spheroid Formation in Central Nervous System Wallerian Degeneration." Journal of Neuropathology & Experimental Neurology 69, no. 5 (May 2010): 455–72. http://dx.doi.org/10.1097/nen.0b013e3181da84db.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

DeFrancesco-Lisowitz, A., J. A. Lindborg, J. P. Niemi, and R. E. Zigmond. "The neuroimmunology of degeneration and regeneration in the peripheral nervous system." Neuroscience 302 (August 2015): 174–203. http://dx.doi.org/10.1016/j.neuroscience.2014.09.027.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

&NA;. "Does Scuba Diving Cause Cervical Disc and Central Nervous System Degeneration?" Back Letter 10, no. 8 (August 1995): 87. http://dx.doi.org/10.1097/00130561-199508000-00005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Zachary, J. F., and D. P. O'Brien. "Spongy Degeneration of the Central Nervous System in Two Canine Littermates." Veterinary Pathology 22, no. 6 (November 1985): 561–71. http://dx.doi.org/10.1177/030098588502200609.

Full text

Abstract:

Progressive dysmetria was observed at four months and six months of age in two female Labrador retriever littermates. Neurological examinations indicated a cerebellar disorder. Laboratory analyses were normal. The dogs were studied clinically until they were killed for necropsy at nine months and eleven months of age. Both dogs had normal brain size, shape, and calvarial symmetry; the older dog had body weight loss, reduced brain weight, and muscle atrophy. Microscopically, there were vacuoles, hypertrophied fibrous astrocytes, myelin loss, and prominent blood vessels, distributed symmetrically in the subcortical and deep white matter of all lobes of the cerebrum; in the folial and deep white matter of the cerebellum; in the tracts of some cranial nerves; in the thalamic area, midbrain and brainstem; and in the white matter of the spinal cord. There was no significant myelinolysis, inflammation, or axonal degeneration. Ultrastructurally, there were intramyelinic vacuoles with separation of lamellae at intraperiod lines and larger spaces formed by coalescence of ruptured vacuoles. Hypertrophied fibrous astrocytes had abundant glial filaments, edematous cytosol, membrane-bound crystalline inclusions, dilated cytocavitary systems, and abnormal mitochondria. The clinical, histological, and ultrastructural findings resembled those reported for the juvenile form of Canavan's disease (van Bogaert and Bertrand type) in children.

APA, Harvard, Vancouver, ISO, and other styles

37

Khosravi, Mahvash, David D. Weaver, Marilyn J. Bull, Ralph Lachman, and David L. Rimoin. "Lethal syndrome of skeletal dysplasia and progressive central nervous system degeneration." American Journal of Medical Genetics 77, no. 1 (April 28, 1998): 63–71. http://dx.doi.org/10.1002/(sici)1096-8628(19980428)77:1<63::aid-ajmg14>3.0.co;2-m.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Ezura, Kazuhiko, Yoshihide Usami, Kazuhiko Tajima, Hideo Komaniwa, Satomi Nagai, Minoru Narita, and Kenji Kawashima. "Gastrointestinal and Skin Lesions in Piglets Naturally Infected with Pseudorabies Virus." Journal of Veterinary Diagnostic Investigation 7, no. 4 (October 1995): 451–55. http://dx.doi.org/10.1177/104063879500700405.

Full text

Abstract:

Pseudorabies virus (PRV) infection was diagnosed in 4 piglets from a litter by immunohistopathologic examination and virus isolation. Three piglets had moderate to severe neuronal degeneration, and PRV antigen was detected in Auerbach's myenteric plexus and Meissner's submucosal plexus of the gastrointestinal tract. One piglet had 2 types of skin lesions. One lesion appeared on the hip and ear and was characterized by ballooning degeneration, necrosis of epithelial cells, and intranuclear inclusion bodies. The other was found on the ear and hematoma-like lesion and was composed of fibrinoid exudation and degenerative connective tissue. PRV antigen was clearly demonstrated in both skin lesions. These results suggested that degeneration of myenteric plexuses might be another characteristic of lesions in PRV-infected pigs and that the virus spreads by interaction between the skin and myenteric plexuses to the central nervous system.

APA, Harvard, Vancouver, ISO, and other styles

39

Chen, Yingying, Nathan J. Coorey, Meixia Zhang, Shaoxue Zeng, Michele C. Madigan, Xinyuan Zhang, Mark C. Gillies, Ling Zhu, and Ting Zhang. "Metabolism Dysregulation in Retinal Diseases and Related Therapies." Antioxidants 11, no. 5 (May 11, 2022): 942. http://dx.doi.org/10.3390/antiox11050942.

Full text

Abstract:

The human retina, which is part of the central nervous system, has exceptionally high energy demands that requires an efficient metabolism of glucose, lipids, and amino acids. Dysregulation of retinal metabolism disrupts local energy supply and redox balance, contributing to the pathogenesis of diverse retinal diseases, including age-related macular degeneration, diabetic retinopathy, inherited retinal degenerations, and Macular Telangiectasia. A better understanding of the contribution of dysregulated metabolism to retinal diseases may provide better therapeutic targets than we currently have.

APA, Harvard, Vancouver, ISO, and other styles

40

Jane, John A., Osward Steward, and Thomas Gennarelli. "Axonal degeneration induced by experimental noninvasive minor head injury." Journal of Neurosurgery 62, no. 1 (January 1985): 96–100. http://dx.doi.org/10.3171/jns.1985.62.1.0096.

Full text

Abstract:

✓ Minor head injury or concussion was produced in experimental animals by an acceleration-deceleration non-impact injury. The animals sustained a brief loss of consciousness and no sequelae were observed. The brains were examined at 7 days by means of the Nauta and Fink-Heimer techniques. Degenerating axons were noted in the inferior colliculus, pons, and dorsolateral medulla. Degeneration was not seen in the subcortical white matter, thus suggesting a primary brain-stem locus for concussion. These findings also suggest that, in some instances, minor head injury or concussion can be associated with organic damage to the central nervous system.

APA, Harvard, Vancouver, ISO, and other styles

41

Miller, John A., Domenica E. Drouet, Leonid M. Yermakov, Mahmoud S. Elbasiouny, Fatima Z. Bensabeur, Michael Bottomley, and Keiichiro Susuki. "Distinct Changes in Calpain and Calpastatin during PNS Myelination and Demyelination in Rodent Models." International Journal of Molecular Sciences 23, no. 23 (December 6, 2022): 15443. http://dx.doi.org/10.3390/ijms232315443.

Full text

Abstract:

Myelin forming around axons provides electrical insulation and ensures rapid and efficient transmission of electrical impulses. Disruptions to myelinated nerves often result in nerve conduction failure along with neurological symptoms and long-term disability. In the central nervous system, calpains, a family of calcium dependent cysteine proteases, have been shown to have a role in developmental myelination and in demyelinating diseases. The roles of calpains in myelination and demyelination in the peripheral nervous system remain unclear. Here, we show a transient increase of activated CAPN1, a major calpain isoform, in postnatal rat sciatic nerves when myelin is actively formed. Expression of the endogenous calpain inhibitor, calpastatin, showed a steady decrease throughout the period of peripheral nerve development. In the sciatic nerves of Trembler-J mice characterized by dysmyelination, expression levels of CAPN1 and calpastatin and calpain activity were significantly increased. In lysolecithin-induced acute demyelination in adult rat sciatic nerves, we show an increase of CAPN1 and decrease of calpastatin expression. These changes in the calpain-calpastatin system are distinct from those during central nervous system development or in acute axonal degeneration in peripheral nerves. Our results suggest that the calpain-calpastatin system has putative roles in myelination and demyelinating diseases of peripheral nerves.

APA, Harvard, Vancouver, ISO, and other styles

42

Yin, Xinghua, Grahame J. Kidd, Nobuhiko Ohno, Guy A. Perkins, Mark H. Ellisman, Chinthasagar Bastian, Sylvain Brunet, Selva Baltan, and Bruce D. Trapp. "Proteolipid protein–deficient myelin promotes axonal mitochondrial dysfunction via altered metabolic coupling." Journal of Cell Biology 215, no. 4 (November 21, 2016): 531–42. http://dx.doi.org/10.1083/jcb.201607099.

Full text

Abstract:

Hereditary spastic paraplegia (HSP) is a neurological syndrome characterized by degeneration of central nervous system (CNS) axons. Mutated HSP proteins include myelin proteolipid protein (PLP) and axon-enriched proteins involved in mitochondrial function, smooth endoplasmic reticulum (SER) structure, and microtubule (MT) stability/function. We characterized axonal mitochondria, SER, and MTs in rodent optic nerves where PLP is replaced by the peripheral nerve myelin protein, P0 (P0-CNS mice). Mitochondrial pathology and degeneration were prominent in juxtaparanodal axoplasm at 1 mo of age. In wild-type (WT) optic nerve axons, 25% of mitochondria–SER associations occurred on extensions of the mitochondrial outer membrane. Mitochondria–SER associations were reduced by 86% in 1-mo-old P0-CNS juxtaparanodal axoplasm. 1-mo-old P0-CNS optic nerves were more sensitive to oxygen-glucose deprivation and contained less adenosine triphosphate (ATP) than WT nerves. MT pathology and paranodal axonal ovoids were prominent at 6 mo. These data support juxtaparanodal mitochondrial degeneration, reduced mitochondria–SER associations, and reduced ATP production as causes of axonal ovoid formation and axonal degeneration.

APA, Harvard, Vancouver, ISO, and other styles

43

Eikelenboom, M. J., B. M. J. Uitdehaag, and A. Petzold. "Blood and CSF Biomarker Dynamics in Multiple Sclerosis: Implications for Data Interpretation." Multiple Sclerosis International 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/823176.

Full text

Abstract:

Background. Disability in multiple sclerosis (MS) is related to neuroaxonal degeneration. A reliable blood biomarker for neuroaxonal degeneration is needed.Objectives. To explore the relationship between cerebrospinal fluid (CSF) and serum concentrations of a protein biomarker for neuroaxonal degeneration, the neurofilaments heavy chain (NfH).Methods. An exploratory cross-sectional (n=51) and longitudinal (n=34) study on cerebrospinal fluid (CSF) and serum NfH phosphoform levels in patients with MS. The expanded disability status scale (EDSS), CSF, and serum levels of NfH-SMI34 and NfH-SMI35 were quantified at baseline. Disability progression was assessed at 3-year followup.Results. At baseline, patients with primary progressive MS (PPMS, EDSS 6) and secondary progressive MS (SPMS, EDSS 6) were more disabled compared to patients with relapsing remitting MS (RRMS, EDSS 2,P<.0001). Serum and CSF NfH phosphoform levels were not correlated. Baseline serum levels of the NfH-SMI34 were significantly (P<.05) higher in patients with PPMS (2.05 ng/mL) compared to SPMS (0.03 ng/mL) and RRMS (1.56 ng/mL). In SPMS higher serum than CSF NfH-SMI34 levels predicted disability progression from baseline (ΔEDSS2,P<.05). In RRMS higher CSF than serum NfH-SMI35 levels predicted disability progression (ΔEDSS2,P<.05).Conclusion. Serum and CSF NfH-SMI34 and NfH-SMI35 levels did not correlate with each other in MS. The quantitative relationship of CSF and serum NfH levels suggests that neuroaxonal degeneration of the central nervous system is the likely cause for disability progression in RRMS. In more severely disabled patients with PP/SPMS, subtle pathology of the peripheral nervous system cannot be excluded as an alternative source for blood NfH levels. Therefore, the interpretation of blood protein biomarker data in diseases of the central nervous system (CNS) should consider the possibility that pathology of the peripheral nervous system (PNS) may influence the results.

APA, Harvard, Vancouver, ISO, and other styles

44

Agnello, Luisa, and Marcello Ciaccio. "Neurodegenerative Diseases: From Molecular Basis to Therapy." International Journal of Molecular Sciences 23, no. 21 (October 25, 2022): 12854. http://dx.doi.org/10.3390/ijms232112854.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Gonzalez, David, and Miguel L. Allende. "Current Advances in Comprehending Dynamics of Regenerating Axons and Axon–Glia Interactions after Peripheral Nerve Injury in Zebrafish." International Journal of Molecular Sciences 22, no. 5 (March 2, 2021): 2484. http://dx.doi.org/10.3390/ijms22052484.

Full text

Abstract:

Following an injury, axons of both the central nervous system (CNS) and peripheral nervous system (PNS) degenerate through a coordinated and genetically conserved mechanism known as Wallerian degeneration (WD). Unlike central axons, severed peripheral axons have a higher capacity to regenerate and reinnervate their original targets, mainly because of the favorable environment that they inhabit and the presence of different cell types. Even though many aspects of regeneration in peripheral nerves have been studied, there is still a lack of understanding regarding the dynamics of axonal degeneration and regeneration, mostly due to the inherent limitations of most animal models. In this scenario, the use of zebrafish (Danio rerio) larvae combined with time-lapse microscopy currently offers a unique experimental opportunity to monitor the dynamics of the regenerative process in the PNS in vivo. This review summarizes the current knowledge and advances made in understanding the dynamics of the regenerative process of PNS axons. By using different tools available in zebrafish such as electroablation of the posterior lateral line nerve (pLLn), and laser-mediated transection of motor and sensory axons followed by time-lapse microscopy, researchers are beginning to unravel the complexity of the spatiotemporal interactions among different cell types during the regenerative process. Thus, understanding the cellular and molecular mechanisms underlying the degeneration and regeneration of peripheral nerves will open new avenues in the treatment of acute nerve trauma or chronic conditions such as neurodegenerative diseases.

APA, Harvard, Vancouver, ISO, and other styles

46

Quinn, Peter M. J., António Francisco Ambrósio, and Celso Henrique Alves. "Oxidative Stress, Neuroinflammation and Neurodegeneration: The Chicken, the Egg and the Dinosaur." Antioxidants 11, no. 8 (August 11, 2022): 1554. http://dx.doi.org/10.3390/antiox11081554.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Sukhanov, S. A., and A. V. Agapov. "On the question of secondary degeneration in the spinal cord." Neurology Bulletin V, no. 2 (October 22, 2020): 102–15. http://dx.doi.org/10.17816/nb47083.

Full text

Abstract:

At the present time, in the method of coloring the nervous system according to Marchi, we have an extremely sensitive reagent, with the help of which it is possible to ascertain early changes in nerve fibers that undergo secondary degeneration for one reason or another. Only with the help of this method more accurate and definite data were obtained regarding the order in which and on which day after the injury of the spinal cord, the degeneration begins in its individual systems.

APA, Harvard, Vancouver, ISO, and other styles

48

Rybachok, Oksana Aleksandrovna. "Multiple sclerosis as one of the causes of disability at a young age." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 11 (October 29, 2021): 26–31. http://dx.doi.org/10.33920/med-10-2111-03.

Full text

Abstract:

Multiple sclerosis is one of the most severe degenerative diseases of the central nervous system and is a variant of autoimmune pathology, in which demyelination and degeneration of nerve fibers occurs, against which there is a violation of their conduction. Its development occurs gradually and has a pronounced staging of the pathological process. The disease occurs as a result of the combined interaction of external factors (viruses, infection, intoxication, dietary characteristics, exposure to stressful situations, poor ecology) and hereditary predisposition. In the world, there are about 3 million patients suffering from various forms of multiple sclerosis. As a result of this pathological process, the central and peripheral nervous system is damaged mainly in young people of working age, which leads to their early disability, limitation of life opportunities, and gives reason to consider this disease a socially significant issue of our time.

APA, Harvard, Vancouver, ISO, and other styles

49

Kovrazhkina, E. A., L. V. Stahovskaya, and O. D. Razinskaya. "Axonal degeneration and secondary demyelization in the central and peripheral nervous system." Consilium Medicum 18, no. 9 (2016): 87–91. http://dx.doi.org/10.26442/2075-1753_2016.9.87-91.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Montagne, Axel, Angeliki M. Nikolakopoulou, Zhen Zhao, Abhay P. Sagare, Gabriel Si, Divna Lazic, Samuel R. Barnes, et al. "Pericyte degeneration causes white matter dysfunction in the mouse central nervous system." Nature Medicine 24, no. 3 (February 5, 2018): 326–37. http://dx.doi.org/10.1038/nm.4482.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!