Relevant bibliographies by topics / Nervous system – Degeneration

Academic literature on the topic 'Nervous system – Degeneration'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Nervous system – Degeneration"

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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.

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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.

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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.

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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.

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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.
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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.

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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.
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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.

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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.

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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.

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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.

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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.)
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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.

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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.
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Dissertations / Theses on the topic "Nervous system – Degeneration"

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Biro, Andrew J. "Specific aspects of neurodegenerative disease." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28919.

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This thesis is broken into four chapters. The first two chapters summarize two separate lines of investigation into the role of a putative neurotoxin in the pathogenesis of Huntington's Disease (HD). The third chapter outlines an investigation of the putative role of beta-N-methylamino-L-alanine (BMAA) in the pathogenesis of amyotrophic lateral sclerosis (ALS), while the final chapter details a post-mortem investigation of the contents of biogenic amines and amino acids in the brain of a man who died of a familial form of parkinsonism. Chapter I is a description of a chromatographic technique developed to isolate quinolinic acid (QA), an endogenous compound implicated in the pathogenesis of HD, from deproteinized human sera. A cation exchange column was used to selectively isolate QA, which was eluted with 10 mM HCl. The eluted fractions were analyzed by UV spectrometry to isolate and quantify QA. Once the fractions corresponding the elution of authentic QA were isolated, concentrated and the excess HCl removed, the fractions were added to growing fetal rat striatal explant cultures as an assay of neurotoxicity. Since HD involves the selective degeneration of GABAergic neurons in the striatum, the activity of glutamic acid decarboxylase, the final enzyme in the synthesis of GABA, was used to determine the viability of the cultures. Unfortunately, the method was confounded by the contamination of all effluents by compounds originating from the cation exchange resin, which were discovered to be neurotoxic to the striatal cultures, and as a result the investigation had to be abandoned. Chapter II describes an investigation designed to further characterize the nature of neurotoxicity observed in the sera obtained from patients with HD (Perry et al. 1987). Compounds with the capacity to selectively stimulate neurons at the N-methyl-D-aspartate (NMDA) receptor have been implicated in a variety of neurodegenerative disorders, including HD. Selective antagonists at the NMDA receptor have been shown to protect neurons from the degenerative effects of such "excitotoxins". The investigation described used MK-801, a potent noncompetitive NMDA antagonist, in an attempt to protect fetal rat striatal cultures from the neurodegenerative effects of the sera obtained from HD patients. The results obtained were equivocal. No evidence was obtained to support a role of the NMDA receptor in the mediation of the neurotoxicity, and in addition the neurodegenerative effects of HD sera were not reproduced in the present investigation. A variety of possible explanations for the apparent discrepancy are suggested. Chapter III describes an experiment intended to produce an animal model of ALS based on the observations by Spencer et al. 1987 that chronic oral administration of BMAA in monkeys produced the histological and behavioural characteristics of this disease. In the present investigation synthetic D,L-BMAA was given by gavage to mice over an eleven week period. Since BMAA is known to act at the NMDA receptor, a subset of the mice were also given MK-801 in an effort to protect them from any deleterious effects based on the action of BMAA at this receptor. The animals were sacrificed at the end of the experiment, and biochemical analyses were performed on the striata and cortices of the animals. In addition, neuropathological studies were performed on the spinal cords, basal ganglia and related structures. The results indicated no biochemical or neuropathological abnormality as a result of BMAA administration. Chapter IV describes a post-mortem investigation of a man who was a member of a well described pedigree which carries an autosomal dominant form of parkinsonism. The object of the investigation was to determine post-mortem levels of dopamine, noradrenaline, serotonin and their metabolites, in addition to amino acids in various regions of brain. Although conflicting evidence was obtained during life, neuropathological findings and the present neurochemical analyses confirm the degeneration of the nigrostriatal dopaminergic tract, characteristic of parkinsonism, in this man.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Babetto, Elisabetta. "Axon degeneration mechanisms in Alzheimer's disease and injury." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609249.

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Godzik, Katharina. "The NAD salvage pathway and Wallerian degeneration." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707906.

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Tsao, Jack W. "Wallerian degeneration in normal mice and in mutant C57BL/Wld mice." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260174.

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Lunn, Elizabeth Ruth. "Studies on the degeneration and regeneration of neurons to skeletal muscle." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292675.

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Hung, Hiu-ling, and 洪曉翎. "Characterization of mitochondrial morphology and dynamics in neurodegeneration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50126362.

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Duan, Rui-Sheng. "Inflammation and neurodegeneration in mouse nervous system: experimental application /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-606-9/.

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Maharaj, Deepa Sukhdev. "An investigation into the physico-chemical and neuroprotective properties of melatonin and 6-hydroxymelatonin." Thesis, Rhodes University, 2003. http://eprints.ru.ac.za/71/.

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Schwarz, Stefan Theodor. "Magnetic resonance imaging correlates of neuronal degeneration of brain stem nuclei in Parkinson's disease." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/37023/.

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Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterised by a loss of pigmented dopaminergic neurons in the substantia nigra (SN) pars compacta and loss of pigmented noradrenergic neurons in the locus coeruleus (LC). Diagnosing PD can be challenging, especially in the early stages particularly when the typical movement disorder symptoms such as tremor, rigidity, bradykinesia and postural instability are not easily identifiable. Despite well-established PD clinical diagnostic criteria there is a misdiagnosis rate of up to 15% by neurology specialists and 25 % by general practitioners. The only approved diagnostic test to confirm suspected PD in a tremulous patient is dopamine transporter single photon emission tomography (DaTScanTM). This test is costly (£800 – 1500 in the UK) and has limited geographical availability in the UK. It involves exposure to ionising radiation and can only be used to assess the integrity of the dopaminergic system. Therefore there is a strong need for better and more accessible diagnostic tests for PD. The aim of this thesis is to investigate the sensitivity and specificity of three different MRI techniques as potential biomarkers of PD. MRI at 3T field strength was used in this thesis to demonstrate PD pathology in the pigmented brain stem nuclei of SN, LC and the ventral tegmental area (VTA). The objective was to develop new, easily accessible and affordable disease markers to help clinicians to establish the correct diagnosis early. A promising technique, which is based on the assessment of free motion of water-associated protons in tissue, is termed diffusion tensor imaging (DTI). The amount of free motion in all directions of protons in tissues like the brain can be described using mean diffusivity (MD) as a measure. Diffusion in tissues like the brain is often limited (“restricted”) in certain directions. For example diffusion across the myelin sheaths of nerve-fibres in the brain white matter is constrained, whereas along the direction of the nerve fibre protons can diffuse freely. This is termed anisotropic diffusion and can be described using fractional anisotropy as a measure (FA). Microstructural PD pathological processes may alter these measures of diffusivity especially in the area of the early affected brain region of the SN. In a prospective case control study of 30 patients and 22 controls diffusion tensor imaging alterations of the SN were investigated by measuring regional alterations of fractional FA and MD. In addition, a systematic literature review and meta-analysis was performed to determine the evidence for nigral DTI alterations throughout the literature. The case control study did demonstrate a small but significant increase of nigral MD; however the meta-analysis did not confirm this result when synthesizing effect sizes of nine identified relevant studies. No significant PD induced FA alterations were found in the prospective case control study. The meta-analysis of nigral FA changes did likewise not show significant FA decrease after correcting for studies with unusual high FA measures in the control arm population. In summary the meta-analysis and the results of the case control study did not confirm that standard DTI measurements of the SN are reliable biomarkers of PD pathology. In a further case-control study MRI sequences tracking the neuromelanin content of the pigmented brain stem nuclei like the SN, LC and the ventral tegmental area were investigated. PD induced decline of neurons in these nuclei causes depigmentation due to loss of neuromelanin content. In this study (including data from 24 PD patients and 20 controls) I found that only little neuromelanin related signal could be observed in the ventral tegmental area and there was no significant difference between patients with PD and controls. However, there were significant signal alterations of the SN and LC signal when comparing between the two groups. The neuromelanin related signal loss was most pronounced in the posterior SN even in the earlier stages of the disease. The signal loss in the anterior SN was less severe and correlated with the unified PD rating scale (UPDRS) and Hoehn and Yahr score as a measure of disease severity. The neuromelanin related signal reduction was significant but less extensive in the region of the LC when compared to the SN. The signal alterations in the LC did not correlate with the UPDRS or the Hoehn and Yahr score. In the third part of the experimental section of this thesis, a further prospective case-control study of 19 participants (10 patients with PD) and retrospective study of 105 clinical cases (9 patients with PD) was performed. A high resolution SWI/T2* ‘iron sensitive’ sequence was used to assess MRI changes of the nigrosome-1. Nigrosomes are little islands of dopaminergic cells with physiologically low iron content. The healthy hyperintense signal of the linear shaped nigrosome-1 surrounded by the iron containing low signal SN regions has great resemblance to the appearance of a swallow tail. The PD induced pathological signal reduction within nigrosome-1 resulted in a loss of the typical ‘swallow tail appearance’. Visual qualitative assessment of the MRI scans for absence and presence of nigrosome-1 revealed high sensitivity and specificity (80-100% and 86-89% respectively) to allow differentiation of PD from healthy controls and non-PD patients. In summary I found that standard nigral DTI is not reliable as a PD biomarker. Nigrosome and neuromelanin weighted MRI offers great potential for development into a clinically useful biomarker. Comparing the two techniques, nigrosome imaging has some advantages over neuromelanin weighted imaging: the high resolution SWI/T2* sequence is shorter (2-5 min versus 7-14 min neuromelanin MRI. However, further optimization of neuromelanin MRI sequences may be able to shorten the acquisition time. A further advantage of nigrosome MRI is that the images can be visually assessed for pathological alterations without the need for complicated analysis or data processing. A disadvantage of high resolution SWI/T2* is that it is more prone to artefacts. An advantage of neuromelanin weighted MRI is that changes especially in the anterior substantia nigra correlate to measures of disease severity like the UPDRS, although there is some early evidence from pilot studies that nigrosome imaging (at field strengths of 7T) may also be useful to assess disease severity related changes. Which of the two techniques is better suited to monitor longitudinal progressive PD related changes has to be assessed in future studies. In conclusion standard nigral DTI measures have no proven value as a reliable diagnostic marker of PD. High resolution T2*/SWI MRI and neuromelanin weighted MRI of PD induced alteration of pigmented brain stem neurons distinguish PD from non-PD and control subjects with high sensitivity and specificity. Neuromelanin related alterations especially of the anterior SN correlate to disease severity measures like the UPDRS and therefore have potential as disease progression marker. The easy applicability of the ‘swallow tail sign’ to indicate a healthy nigrosome-1 in the SN may well prove a useful marker to help the clinical diagnosis of PD. If future studies confirm a similar diagnostic accuracy as the current clinical gold standard DaTScanTM, nigrosome MRI may replace DaTScanTM in the standard clinical setting.
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Hughes, P. M. "Role of matrix metalloproteinases in inflammatory demyelination of the peripheral nervous system." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390492.

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Books on the topic "Nervous system – Degeneration"

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1938-, Saunders Norman, and Dziegielewska Katarzyna M. 1949-, eds. Degeneration and regeneration in the nervous system. Australia: Harwood Academic, 2000.

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Dziegielewska, K. M., Anatomy Physiology, and Physiology. Degeneration and Regeneration in the Nervous System. Edited by N. R. Saunders. Abingdon, UK: Taylor & Francis, 1991. http://dx.doi.org/10.4324/9780203304488.

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B, Caine Donald, ed. Neurodegenerative diseases. Philadelphia: W.B. Saunders Co., 1994.

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Cajal's degeneration and regeneration of the nervous system. New York: Oxford University Press, 1991.

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I, Tröster Alexander, ed. Memory in neurodegenerative disease: Biological, cognitive, and clinical perspectives. Cambridge, UK: Cambridge University Press, 1998.

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Neurodegenerative diseases. Austin, Tex: Landes Bioscience, 2011.

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E, Ribak Charles, ed. From development to degeneration and regeneration of the nervous system. New York: Oxford University Press, 2009.

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Kim, Hŭi-sŏn. Noe sogyo sepʻo esŏ isoflavones ŭi hangyŏmchŭng chagyong kijŏn kyumyŏng mit noe chirhwan chʻiryo e ŭngyong =: Identification of anti-inflammatory mechanism of isoflavones in brain microglia and application to treatment of neurodegenerative diseases. [Seoul]: Pogŏn Pokchibu, 2007.

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Aging and the nervous system. Chichester: John Wiley & Sons, 1988.

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Flint, Beal M., Lang Anthony E, and Ludolph Albert C, eds. Neurodegenerative diseases: Neurobiology, pathogenesis, and therapeutics. Cambridge, UK: Cambridge University Press, 2005.

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Book chapters on the topic "Nervous system – Degeneration"

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Koeppen, Arnulf H. "Wallerian Degeneration." In Alterations of Metabolites in the Nervous System, 443–506. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-6740-7_17.

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Hosokawa, Masato, and Tetsuaki Arai. "Progranulin and Frontotemporal Lobar Degeneration." In Progranulin and Central Nervous System Disorders, 35–69. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6186-9_3.

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Schallert, Timothy, and Jennifer L. Tillerson. "Intervention Strategies for Degeneration of Dopamine Neurons in Parkinsonism." In Central Nervous System Diseases, 131–51. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-691-1_8.

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Spencer, Peter S., Matthew S. Miller, Stephen M. Ross, Bradley W. Schwab, and Mohammad I. Sabri. "Biochemical Mechanisms Underlying Primary Degeneration of Axons." In Alterations of Metabolites in the Nervous System, 31–65. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-6740-7_2.

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Schweizer, Ulrich. "Selenoproteins in Nervous System Development, Function and Degeneration." In Selenium, 427–39. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41283-2_36.

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Schweizer, Ulrich. "Selenoproteins in Nervous System Development, Function, and Degeneration." In Selenium, 235–48. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1025-6_18.

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Miller, Freda D., and David R. Kaplan. "Nervous System Aging, Degeneration, and the p53 Family." In Research and Perspectives in Alzheimer's Disease, 83–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-16602-0_7.

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Reier, Paul J., and Michael A. Lane. "Degeneration, Regeneration, and Plasticity in the Nervous System." In Neuroscience in Medicine, 691–727. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-455-5_46.

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Reier, Paul J., and Margaret J. Velardo. "Degeneration, Regeneration, and Plasticity in the Nervous System." In Neuroscience in Medicine, 663–701. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-371-2_32.

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Sanchez-Dalmau, Bernardo F., Ruben Torres-Torres, Johannes Keller, Elena H. Martínez-Lapiscina, and Pablo Villoslada. "Trans Neuronal Retrograde Degeneration to OCT in Central Nervous System Diseases." In OCT in Central Nervous System Diseases, 205–14. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24085-5_11.

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Conference papers on the topic "Nervous system – Degeneration"

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Fournier, Adam, Suneil Hosmane, and K. T. Ramesh. "Thresholds for Embryonic CNS Axon Integrity, Degeneration, and Regrowth Using a Focal Compression Platform." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80331.

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Traumatic axonal injuries (TAI) are broadly defined as the focal or multi-focal damage of axons within white matter tracts of the central nervous system (CNS), and can occur in the setting of spinal cord injury (SCI) and traumatic brain injury (TBI). TAI can result from mechanical forces associated with the rapid deformation of white matter regions during trauma. Through combinations of compression, stretch, and shear, axon injury often results in an irreversible loss of functional neural connectivity, since the scope for axonal regeneration in the CNS is extremely limited.
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Borges, Isabella Sabião, João Victor Aguiar Moreira, Eustaquio Costa Damasceno Junior, Alencar Pereira dos Santos, Gabriela Tomás Alves, Leonardo Peixoto Garcia, Maria Fernanda Prado Rosa, et al. "Chronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.413.

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Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.
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Andrade, Gabriel Costa Ferreira. "Deep brain stimulation for treatment of Parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.665.

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Introduction: Parkinson’s disease (PD) is a degenerative and chronic disorder that affects the central nervous system. It occurs due to the degeneration of neurons in the ventral layer of the compact part of the substance nigra and the locus ceruleus, for reasons still unknown. As a result, there is a decrease in dopamine, causing the classic manifestations of the disease, mainly motor. Deep Cerebral Stimulation (ECP) is a therapeutic modality that emerged in the 1980s and has achieved quite satisfactory results in the treatment of PD, especially in more advanced cases and / or refractory to drug treatment. Objectives: To analyze the effectiveness of ECP for the treatment of PD. Methodology: This study consists of an integrative review through the selection of eight articles published randomly between 2017 and 2021 on the platforms PubMed and Google Scholar, using the descriptors “Parkinson’s Disease” and “Deep Brain Stimulation” in the English and Portuguese languages. Results: It is seen that the symptoms of PD are related to the reduction of activation of areas such as motor cortex, substance nigra and globe palidum. In this sense, ECP uses the application of constant or intermittent electrical current, of low intensity and high frequency. Such a stimulus is capable of inhibiting the activity of the subthalamic nucleus or pale globe, among other regions, resulting in significant improvement of symptoms. On the other hand, some recent studies have identified a risk, albeit low, of post-procedure movement limitations, deaths from infections and increased suicides. Conclusion: There was an improvement in physical symptoms, as well as a significant decrease in the frequency of dementia, depression and psychological problems, with the ECP being a safe and effective procedure for the treatment of PD.
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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa, and Edvaldo Cardoso. "Brain-gut-microbiota axis in motor disorders." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.401.

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Introduction: There seems to be a strong relationship and influence on the brain-gut- microbiota axis in the control and prevention of several diseases, including degenerative diseases that are related to motor disorders. Objectives: To analyze the relationship between movement disorders and the intestinal microbiota. Methods: Integrative review performed at PUBMED, using the descriptors Movement disorder and intestinal microbiota, in the last five years and having as inclusion criteria complete texts in English. Results: The literature suggests that the intestinal microbiota regulates the activation of microglia through the production of bacteria metabolites. Gut dysbiosis is believed to generate metabolic disorders with decreased production of neuroprotective factors, increased pro-inflammatory cytokines, production of neurotoxins, and a misdirected immune response. Metabolites produced by an altered microbiota seem to enter the circulation and affect neurological function. Braak’s hypothesis postulates that aberrant accumulation of α-synuclein (αSyn), a central component of the pathophysiology of Parkinson’s disease (PD), begins in the intestine and propagates through the vagus nerve to the brain, given that αSyn inclusions previously arise in the enteric nervous system and glossopharyngeal and vagus nerves, and vagotomized individuals have reduced risk of PD. Conclusion: The identification of the microbiota or its altered metabolites may serve as biomarkers, or even drug targets for the treatment of diseases of the central nervous system. The microbiota can be modulated through antibiotic therapy, fecal microbiota transplantation, prebiotic supplementation, dietary interventions and many other potential methods.
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Kim, Jung Hwan, Garrett W. Astary, Thomas H. Mareci, and Malisa Sarntinoranont. "A Computational Model of Direct Infusion Into the Rat Brain: Corpus Callosum and Hippocampus." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205945.

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Despite the high therapeutic potential of many macromolecular drugs, it has proven difficult to apply them to treatment of cancer and other degenerative diseases of the central nervous system (CNS) due to low capillary permeability and low diffusivity. To overcome these barriers, recent experimental studies have shown local infusion, i.e., convection-enhanced delivery (CED), to be a promising delivery technique in the brain and spinal cord [1–3]. Predictive models of extracellular fluid flow and transport during CED would be useful for treatment optimization and planning.
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Shah, Vrutangkumar V., Sachin Goyal, and Harish Palanthandalam-Madapusi. "A Biomechanical Approach to Diagnosis and Monitoring of Parkinson’s Disease." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-46781.

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Parkinson’s disease is an idiopathic and degenerative disorder of the central nervous system. Among the symptoms, the tremor at rest is one of the prominent symptoms. The challenge however is that there are no definitive diagnostic test that can confirm the presence or severity of Parkinson’s disease. This is a serious handicap especially since the drugs usually prescribed to control these symptoms have serious side effects and their dosages have to be tuned extensively. Also, the exact origin of tremor is unknown. There have been recent efforts [19] to understand the mechanism behind the Parkinsonian tremor, from a control-system perspectives. From these efforts, it appears that increased sensorimotor loop delay may be a cause for Parkinsonian tremor and thus serve as a key distinguishing feature. In the current work, we adopted this hypothesis and with the help of a relatively straightforward analysis of the motor control loop along with the help of some simulation and experimental examples, we first attempt to explain several qualitative observations relating to Parkinson’s Disease. Further, we explore the possibilities of for progress tracking, diagnosis, and early diagnosis before onset of tremor using biomechanical means.
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Sirwan Raza, Rzgar, and Adil Hussein Mohammed. "Diagnosis of Parkinson's disease through EEG signals based on artificial neural network and cuckoo search algorithm." In 4th International Conference on Communication Engineering and Computer Science (CIC-COCOS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/cocos2022/paper.698.

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Parkinson's disease is a degenerative nervous system condition that impairs mobility. If the condition is not detected early enough, it might have permanent effects for the sufferer. A novel approach for identifying Parkinson's disease is provided in this research, which employs machine optimization and learning techniques. The suggested method's diagnosis procedure may be broken down into three primary steps: "preprocessing," "feature extraction," and "classification." Preprocessing the EEG data is the initial stage in the suggested technique. Database samples are treated using discrete wavelet analysis to remove the destructive influence of noise on the input signals using signal analysis for this aim. The suggested method's second phase will employ principal component analysis to remove duplicate features and minimize data dimensionality. The artificial neural network model is trained and the classification model is built using the retrieved features. The effectiveness of the suggested technique is examined in terms of criteria such as accuracy, sensitivity, and specificity during the experimentation phase, and the results are compared to existing learning models. The findings revealed that the suggested technique enhances illness diagnostic accuracy by at least 8.25% and may be utilized as a useful tool in disease diagnosis.
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Aquino, Letícia, Juliana Victor dos Santos, Jaqueline Donola Scandoleira, Jéssica Elen Gonçalves Nascimento, and Letícia Moraes de Aquino. "Telerehabilitation in Amyotrophic Lateral Sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.528.

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Introduction: Amyotrophic Lateral Sclerosis (ALS) is a progressive and degenerative motor disease of the nervous system. Symptoms are variable, the main one being muscle weakness. Treatment is based on medication and monitoring by a multidisciplinary team to maintain quality of life (QoL) and autonomy. There are barriers, like mobility, and telehealth (TH) can be a possibility of care. Objectives: To identify evidence of the use of TH in patients with ALS to improve symptoms and QoL. Design and settings: Study carried out at Centro Universitario São Camilo. Methodology: Literature review in the PubMed, Lilacs and PEDro, between 2011 and 2021, in Portuguese, English or Spanish, with “ALS”, “telemedicine”, “TH”. Results: Of the 14 studies found, 13 were selected after review. The majority (93%) made use of video and telephone calls for monitoring and new orientations, after face-to-face evaluation; but all showed the possibility of remote assessment, associated or no with technological resources (such apps, accelerometers, smartwatches). 31% of the studies reported indication of TH for respiratory care in critically ill patients. In general, 93% of the papers demonstrated that TH brought benefits in maintaining QoL and improving respiratory parameters. Conclusion: Use of TH in patients with ALS seems to be to viable, safe and beneficial for assessment and monitoring, especially in advanced stages and for respiratory symptoms.
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Santos, Antônio Henrique Roberti dos, Bruno Costa Barbosa, Gabriela Resmini Durigon, and Guilherme Neumann de Araújo. "Analytical study of the evolution of hospitalizations for Parkinson’s disease in comparison with the region, race, sex and age range in Brazil in the last 10 years." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.320.

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Background: Parkinson’s disease is a chronic and degenerative central nervous system neuropathy, caused by decrease of the dopamin hormone. The therapy is symptomatic, neuroprotective and restorative, however it´s still very disabling in advanced stages. Objectives: Report the number of cases of the disease in different social sectors, to establish link between etiology and health promotion. Methods: An analytical epidemiological study carried out by research at DATASUS that analyzes the number of Brazilians admissions for Parkinson’s Disease, between January/2011 to December/2020, associating these to the incidence according to age group, race, region and sex. Results: Observing Brazil’s hospitalizations, since 2011, due to Parkinson’s Disease, noticed: 9,210 cases, being 5,303 (57.58%) male. In the regional proportion, Southeast had the highest incidence with 4,050 cases, followed by South with 2,470, Northeast with 1,800, Midwest with 519 and North with 371. Segregating in states, São Paulo had the highest number 2239, followed by Rio Grande do Sul with 1155. Regarding race, whites with 4,355 cases had the highest incidence, followed by browns with 1825. In the proportion curve between 2011-2020, there’s reduction of approximately 1,012% of the registered average. Assessing the age group, there’s higher incidence between 70-79 years followed by 60-69 years. Conclusions: It’s noted that the incidence of Brazilian hospitalizations for Parkinson’s Disease has increased substantially since 2011. Furthermore, the numbers described are hospitalizations, reflecting higher numbers if the total cases are evaluated, in addition to underreporting. So, it’s necessary to invest in methods for early diagnosis seeking to improve the prognosis.
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Reports on the topic "Nervous system – Degeneration"

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Ni, Jiachun, Qiong Jiang, Gang Mao, Yi Yang, Qin Wei, Changcheng Hou, Xiangdong Yang, Wenbin Fan, and Zengjin Cai. The effectiveness and safety of acupuncture for constipation associated with Parkinson’s disease: Protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0091.

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Review question / Objective: Is acupuncture a safe and effective therapy for constipation associated with Parkinson’s disease? Our aim is to assess the effectiveness and safety of acupuncture for constipation associated with PD and give guidance to future research direction. Condition being studied: Parkinson’s disease (PD) is a prevalent degenerative disease of nervous system characterized mainly by static tremor, bradykinesia, myotonia, postural gait disorders and other non-motor symptoms. According to variations on race, ethnicity, age and sex, the incidence of PD ranges from 8 to 20.5 per 100, 000 individuals annually. One global research shows that there were 6.1 million individuals suffer from PD in 2016 and will be 12 million patients around the world. According to several outcomes of case-control studies, the prevalence of constipation in PD varies from 28% to 61%. Constipation, as a common gastrointestinal disease which refers to the clinical presentation of reduced spontaneous complete bowel movement, dyschezia, feeling of incomplete defecation and outlet obstruction, is demonstrated to antedate the motor symptom and it's severity is related to the progression of PD. Acupuncture has been proved to act on the pathogenesis of constipation associated with PD. The proposed systematic review we're about to present is the first advanced evidence-based medical evidence in this area.
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