Academic literature on the topic 'Neuronal cell loss'
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Journal articles on the topic "Neuronal cell loss"
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Fricker, Michael, Aviva M. Tolkovsky, Vilmante Borutaite, Michael Coleman, and Guy C. Brown. "Neuronal Cell Death." Physiological Reviews 98, no. 2 (April 1, 2018): 813–80. http://dx.doi.org/10.1152/physrev.00011.2017.
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Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced. The concept of cell death used to be simple as there were just two or three types, so we just had to work out which type was involved in our particular pathology and then block it. However, we now know that there are at least a dozen ways for neurons to die, that blocking a particular mechanism of cell death may not prevent the cell from dying, and that non-neuronal cells also contribute to neuronal death. We review here the mechanisms of neuronal death by intrinsic and extrinsic apoptosis, oncosis, necroptosis, parthanatos, ferroptosis, sarmoptosis, autophagic cell death, autosis, autolysis, paraptosis, pyroptosis, phagoptosis, and mitochondrial permeability transition. We next explore the mechanisms of neuronal death during development, and those induced by axotomy, aberrant cell-cycle reentry, glutamate (excitoxicity and oxytosis), loss of connected neurons, aggregated proteins and the unfolded protein response, oxidants, inflammation, and microglia. We then reassess which forms of cell death occur in stroke and Alzheimer’s disease, two of the most important pathologies involving neuronal cell death. We also discuss why it has been so difficult to pinpoint the type of neuronal death involved, if and why the mechanism of neuronal death matters, the molecular overlap and interplay between death subroutines, and the therapeutic implications of these multiple overlapping forms of neuronal death.
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Sugawara, Mitsuru, Gabriel Corfas, and M. Charles Liberman. "Influence of Supporting Cells on Neuronal Degeneration After Hair Cell Loss." Journal of the Association for Research in Otolaryngology 6, no. 2 (June 2005): 136–47. http://dx.doi.org/10.1007/s10162-004-5050-1.
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Smith, Ruben, Hinfan Chung, Sara Rundquist, Marion L. C. Maat-Schieman, Lesley Colgan, Elisabet Englund, Yong-Jian Liu, et al. "Cholinergic neuronal defect without cell loss in Huntington's disease." Human Molecular Genetics 15, no. 21 (September 20, 2006): 3119–31. http://dx.doi.org/10.1093/hmg/ddl252.
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Takács-Vellai, Krisztina, Andrew Bayci, and Tibor Vellai. "Autophagy in neuronal cell loss: a road to death." BioEssays 28, no. 11 (2006): 1126–31. http://dx.doi.org/10.1002/bies.20489.
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Abad-Rodriguez, Jose, Maria Dolores Ledesma, Katleen Craessaerts, Simona Perga, Miguel Medina, Andre Delacourte, Colin Dingwall, Bart De Strooper, and Carlos G. Dotti. "Neuronal membrane cholesterol loss enhances amyloid peptide generation." Journal of Cell Biology 167, no. 5 (December 6, 2004): 953–60. http://dx.doi.org/10.1083/jcb.200404149.
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Recent experimental and clinical retrospective studies support the view that reduction of brain cholesterol protects against Alzheimer's disease (AD). However, genetic and pharmacological evidence indicates that low brain cholesterol leads to neurodegeneration. This apparent contradiction prompted us to analyze the role of neuronal cholesterol in amyloid peptide generation in experimental systems that closely resemble physiological and pathological situations. We show that, in the hippocampus of control human and transgenic mice, only a small pool of endogenous APP and its β-secretase, BACE 1, are found in the same membrane environment. Much higher levels of BACE 1–APP colocalization is found in hippocampal membranes from AD patients or in rodent hippocampal neurons with a moderate reduction of membrane cholesterol. Their increased colocalization is associated with elevated production of amyloid peptide. These results suggest that loss of neuronal membrane cholesterol contributes to excessive amyloidogenesis in AD and pave the way for the identification of the cause of cholesterol loss and for the development of specific therapeutic strategies.
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Kranenburg, O., V. Scharnhorst, A. J. Van der Eb, and A. Zantema. "Inhibition of cyclin-dependent kinase activity triggers neuronal differentiation of mouse neuroblastoma cells." Journal of Cell Biology 131, no. 1 (October 1, 1995): 227–34. http://dx.doi.org/10.1083/jcb.131.1.227.
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Studies on the molecular mechanisms underlying neuronal differentiation are frequently performed using cell lines established from neuroblastomas. In this study we have used mouse N1E-115 neuroblastoma cells that undergo neuronal differentiation in response to DMSO. During differentiation, cyclin-dependent kinase (cdk) activities decline and phosphorylation of the retinoblastoma gene product (pRb) is lost, leading to the appearance of a pRb-containing E2F DNA-binding complex. The loss of cdk2 activity is due to a decrease in cdk2 abundance whereas loss of cdk4 activity is caused by strong association with the cdk inhibitor (CKI) p27KIP1 and concurrent loss of cdk4 phosphorylation. Moreover, neuronal differentiation can be induced by overexpression of p27KIP1 or pRb, suggesting that inhibition of cdk activity leading to loss of pRb phosphorylation, is the major determinant for neuronal differentiation.
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Oue, Hiroshi, Yasunari Miyamoto, Shinsuke Okada, Katsunori Koretake, Cha-Gyun Jung, Makoto Michikawa, and Yasumasa Akagawa. "Tooth loss induces memory impairment and neuronal cell loss in APP transgenic mice." Behavioural Brain Research 252 (September 2013): 318–25. http://dx.doi.org/10.1016/j.bbr.2013.06.015.
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Korwitz, Anne, Carsten Merkwirth, Ricarda Richter-Dennerlein, Simon E. Tröder, Hans-Georg Sprenger, Pedro M. Quirós, Carlos López-Otín, Elena I. Rugarli, and Thomas Langer. "Loss of OMA1 delays neurodegeneration by preventing stress-induced OPA1 processing in mitochondria." Journal of Cell Biology 212, no. 2 (January 18, 2016): 157–66. http://dx.doi.org/10.1083/jcb.201507022.
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Proteolytic cleavage of the dynamin-like guanosine triphosphatase OPA1 in mitochondria is emerging as a central regulatory hub that determines mitochondrial morphology under stress and in disease. Stress-induced OPA1 processing by OMA1 triggersmitochondrial fragmentation, which is associated with mitophagy and apoptosis in vitro. Here, we identify OMA1 as a critical regulator of neuronal survival in vivo and demonstrate that stress-induced OPA1 processing by OMA1 promotes neuronal death and neuroinflammatory responses. Using mice lacking prohibitin membrane scaffolds as a model of neurodegeneration, we demonstrate that additional ablation of Oma1 delays neuronal loss and prolongs lifespan. This is accompanied by the accumulation of fusion-active, long OPA1 forms, which stabilize the mitochondrial genome but do not preserve mitochondrial cristae or respiratory chain supercomplex assembly in prohibitin-depleted neurons. Thus, long OPA1 forms can promote neuronal survival independently of cristae shape, whereas stress-induced OMA1 activation and OPA1 cleavage limit mitochondrial fusion and promote neuronal death.
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Tang, Damu, Isao Matsuura, Jerry H. Wang, Ki-Young Lee, and Zhong Qi. "Neuronal Cdc2-like kinase: from cell cycle to neuronal function." Biochemistry and Cell Biology 74, no. 4 (July 1, 1996): 419–29. http://dx.doi.org/10.1139/o96-046.
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Neuronal Cdc2-like kinase, Nclk, is a heterodimer of cyclin-dependent protein kinase 5 (Cdk5) and a 25-kDa essential regulatory subunit that is derived from a 35-kDa brain- and neuron-specific protein. This protein is called neuronal Cdk5 activator, p25/35nck5a. Nclk is one of the best characterized Cdc2 family kinases whose primary function is not cell cycle related. It has been suggested that this protein kinase plays important roles in neurocytoskeleton dynamics and its loss of regulation has been implicated in Alzheimer pathology. As a member of the Cdc2-like kinase family, Nclk shares many common properties with other members of the Cdc2-like kinase family. It also possesses unique characteristics that may be related to its distinct and noncell cycle related functions. The regulatory and functional properties of Nclk are reviewed in this communication.Key words: Cdc2 kinase, Cdk5, neuronal Cdk5 activator.
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Lu, Jian-Qiang, Trevor A. Steve, Matt Wheatley, and Donald W. Gross. "Immune Cell Infiltrates in Hippocampal Sclerosis: Correlation With Neuronal Loss." Journal of Neuropathology & Experimental Neurology 76, no. 3 (March 2017): 206–15. http://dx.doi.org/10.1093/jnen/nlx001.
Full textDissertations / Theses on the topic "Neuronal cell loss"
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Brown, Deborah A. "Mechanisms of neurodegeneration and neuronal cell loss in the hippocampus in murine scrapie." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4422.
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Transmissible spongiform encephalopathies (TSEs) or prion diseases are defined by infectivity and by the pathological damage they produce in the central nervous system (CNS), typically involving spongiform degeneration or vacuolation, deposition of abnormal PrP (PrPSc), glial activation and neuronal loss. Much of our understanding of the TSEs has derived from the study of murine scrapie models. The molecular basis of pathological changes is not clear, in particular the relationship between the deposition of PrPSc and neuronal dysfunction. A typical feature of TSE disease is neuronal loss, although the mechanisms leading to this loss are poorly understood. Apoptosis has been proposed as an important mechanism of TSE associated cell death, but which pathways are involved are still to be determined. The main aims of this thesis are to investigate the progression of the characteristic neuropathological changes observed in the TSE infected brain and to analyse the mechanisms involved in neuronal loss. In this study two contrasting scrapie mouse models were used : the ME7/CV model , and the 87V/VM model in which neuronal loss is targeted to different areas of the hippocampus, the CA1, and CA2 respectively. The role of the caspase-dependent pathway of apoptosis in the neuronal loss was investigated. The results of analysis of pro-apoptotic markers of disease in the two scrapie mouse models differed. The results observed in the ME7/CV scrapie mouse model suggest that apoptosis may not be the main mechanism of neuronal loss, whereas the 87V/VM model showed some indication that apoptosis may be involved. Detailed studies in the progression of neurodegenerative changes in the ME7/CV scrapie mouse model revealed that the initial pathological change observed in the hippocampus was the deposition of PrPSc followed by a glial response, spongiform change and subsequent neuronal degeneration. The role of the cytoskeleton and synaptic dysfunction in the neuronal damage observed in the CA1 of the ME7 infected hippocampus was analysed. Cytoskeletal disruption was observed in the post-synaptic dendritic spine, and the apical dendrites of CA1 neurons at 160days, a time point at which neurons are known to be lost. Changes in the expression of the pre-synaptic protein, synaptophysin and the post-synaptic protein PSD-95 were not observed until the terminal stage of disease when the neuronal loss is profound. In conclusion, this research suggests that the mechanisms of neuronal loss may follow different biochemical pathways, which might not necessarily involve an apoptotic mechanism. Cytoskeletal disruption in the post-synaptic dendritic spine plays a major role in the neuronal dysfunction observed in ME7 infected CA1 neurons, although the post synaptic density does not seem to be involved .Pre-synaptic changes and disruption to the innervation of CA1 neurons is not apparent until the end stages of disease. The trigger for this cytoskeletal disruption and the subsequent neuronal loss may be the early deposition of PrPSc in the extracellular space but the precise mechanisms involved are still to be elucidated. The identification of the key events involved in the mechanisms of neruodegeneration in TSE diseases may lead to the development of therapeutic strategies to inhibit the neurodegenerative process.
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Suzzi, Stefano. "Loss of lrrk2 impairs dopamine catabolism, cell proliferation, and neuronal regeneration in the zebrafish brain." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-229200.
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Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are a major cause of Parkinson’s disease (PD), which is why modelling PD by replicating effects in animal models attracts great interest. However, the exact mechanisms of pathogenesis are still unclear. While a gain-of-function hypothesis generally receives consensus, there is evidence supporting an alternative loss-of-function explanation. Yet, neither overexpression of the human wild-type LRRK2 protein or its pathogenic variants, nor Lrrk2 knockout recapitulates key aspects of human PD in rodent models. Furthermore, there is conflicting evidence from morpholino knockdown studies in zebrafish regarding the extent of zygotic developmental abnormalities.
Because reliable null mutants may be useful to infer gene function, and because the zebrafish is a more tractable laboratory vertebrate system than rodents to study disease mechanisms in vivo, clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9) genomic editing was used to delete the ~60-kbp-long zebrafish lrrk2 locus containing the entire open reading frame. Constitutive removal of both the maternal and the zygotic lrrk2 function (mzLrrk2 individuals) causes a pleomorphic phenotype in the larval brain at 5 days post-fertilisation (dpf), including increased cell death, delayed myelination, and reduced and morphologically abnormal microglia/leukocytes. However, the phenotype is transient, spontaneously attenuating or resolving by 10 dpf, and the mutants are viable and fertile as adults. These observations are mirrored by whole-larva transcriptome data, revealing a more than eighteen-fold drop in the number of differentially expressed genes in mzLrrk2 larvae from 5 to 10 dpf.
Additionally, analysis of spontaneous swimming activity shows hypokinesia as a predictor of Lrrk2 protein deficiency in larvae, but not in adult fish.
Because the catecholaminergic (CA) neurons are the main clinically relevant target of PD in humans, the CA system of larvae and adult fish was analysed on both cellular and metabolic level. Despite an initial developmental delay at 5 dpf, the CA system is structurally intact at 10 dpf and later on in adult fish aged 6 and 11 months. However, monoamine oxidase (Mao)-dependent degradation of biogenic amines, including dopamine, is increased in older fish, possibly suggesting impaired synaptic transmission or a leading cause of cell damage in the long term.
Furthermore, decreased mitosis rate in the larval brain was found, in the anterior portion only at 5 dpf, strongly and throughout the whole organ at 10 dpf. Conceivably, lrrk2 may have a more general role in the control of cell proliferation during early development and a more specialised one in the adult stage, possibly conditional, for example upon brain damage. Because the zebrafish can regenerate lost neurons, it represents a unique opportunity to elucidate the endogenous processes that may counteract neurodegeneration in a predisposing genetic background. To this aim, the regenerative potential of the adult telencephalon upon stab injury was tested in mzLrrk2 fish. Indeed, neuronal proliferation was reduced, suggesting that a complete understanding of Lrrk2 biology may not be fully appreciated without recreating challenging scenarios.
To summarise, the present results demonstrate that loss of lrrk2 has an early effect on zebrafish brain development that is later often compensated. Nonetheless, perturbed aminergic catabolism, and specifically increased Mao-dependent aminergic degradation, is reported for the first time in a LRRK2 knockout model. Furthermore, a link between Lrrk2 and the control of basal cell proliferation in the brain, which may become critical under challenging circumstances such as brain injury, is proposed. Future directions should aim at exploring which brain cell types are specifically affected by the mzLrrk2 hypoproliferative phenotype and the resulting consequences on a circuitry level, particularly in very old fish (i.e., over 2 years of age).
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Suzzi, Stefano [Verfasser], Michael [Akademischer Betreuer] Brand, and Gerd [Gutachter] Kempermann. "Loss of lrrk2 impairs dopamine catabolism, cell proliferation, and neuronal regeneration in the zebrafish brain / Stefano Suzzi ; Gutachter: Michael Brand, Gerd Kempermann ; Betreuer: Michael Brand." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-229200.
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Suzzi, Stefano [Verfasser], Michael [Akademischer Betreuer] [Gutachter] Brand, and Gerd [Gutachter] Kempermann. "Loss of lrrk2 impairs dopamine catabolism, cell proliferation, and neuronal regeneration in the zebrafish brain / Stefano Suzzi ; Gutachter: Michael Brand, Gerd Kempermann ; Betreuer: Michael Brand." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://d-nb.info/114073525X/34.
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Todd, Michael. "The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia: A long-term ischemia maturation study." Thesis, University of Ottawa (Canada), 1998. http://hdl.handle.net/10393/4230.
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We investigated the effects of varying ischemia and survival times on CA1 neuronal loss. Histological analysis of the hippocampus was performed at 2, 7, 14, 28 and 90 days following 3, 5, 7, 10 and 13 minutes of global forebrain ischemia. Our results indicate that the ischemic maturation process extends beyond 7 days. Ten and thirteen minutes of ischemia produced a significant degree of cell loss by 7 days (70.53% and 83.25% respectively), while average cell death at 90 days survival was approximately 12% higher. Most strikingly, seven minutes of ischemia produced approximately 30% CA1 cell loss at 90 days compared to only 3% cell loss at 7 days, a nine-fold increase. No cell loss was observed at 2 and 7 days survival following 5 minutes of ischemia, but an average of 5.6% cell loss was observed at 3 months. Three minutes of ischemia produced no cell damage. Data collapsed over ischemic severity suggested that there may 2 rates of cell death evident in this study: (1) a rapid cell loss occurring within the first 7 days of ischemia and (2) a slow progressive cell loss occurring over weeks. Ten and thirteen minutes of ischemia possessed the rapid cell death, while 7 minutes appeared to display only slow progressive cell loss. The fact that the ischemic maturation process extends well beyond 7 days and that mild ischemia severities can produce significant cell loss at long survival times holds important implications for drug trials and our current knowledge of death mechanisms. (Abstract shortened by UMI.)
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Todd, Mike. "The effects of multiple ischemia and survival times on hippocampal CA1 neuronal cell loss in a rat model of global ischemia, a long-term ischemia maturation study." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36746.pdf.
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Bezuidenhout, Lois-Mary. "Triquinylamines as regulators of calcium homeostasis of neuronal cells / Lois-Mary Bezuidenhout." Thesis, North-West University, 2007. http://hdl.handle.net/10394/1470.
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Voisin, Jessica. "Rôle de FOXO3 dans la régulation des phases précoces de la maladie de Huntington lors de la différenciation neuronale." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066613/document.
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FOXO3 est un facteur de transcription important pour la réponse au stress, la régulation de la différenciation et de la survie cellulaires qui a des effets neuroprotecteurs dans plusieurs modèles de maladies neurodégénératives, dont la maladie de Huntington (MH). Les effets neuroprotecteurs de FOXO3 sont réprimés dans la MH par une activité anormale de Ryk, un récepteur Wnt important pour la neurogenèse, par la liaison du domaine intracellulaire de Ryk à la ?-caténine, un co-facteur de FOXO3. L'objectif principal de ce travail est d'étudier les effets de la huntingtine mutée (mHTT) sur le répertoire des cibles directes humaines de FOXO3 à l'aide d'un modèle des phases développementales de la MH, à savoir des cellules souches neurales isogéniques issues de cellules souches pluripotentes induites. En formant un complexe tripartite avec la ?-caténine et FOXO3, Ryk agit comme un co-régulateur de FOXO3 en conditions normales ou pathologiques. L'analyse des cibles directes de FOXO3 montre une reprogrammation de ces cibles avec des pertes et des gains dans des voies de signalisation qui sont connues pour leur rôle dans la MH, notamment les voies de régulation de la prolifération cellulaire. Ces résultats montrent que la régulation des gènes par FOXO3 est fortement modifiée dans les cellules qui expriment la mHTT. Cela ouvre la voie à l'étude des mécanismes d'homéostase cellulaire sous contrôle de FOXO3 dans les neurones en différenciation et leur impact sur l'activité des neurones adultes. Plus largement, ces résultats permettent de mieux comprendre la dynamique moléculaire de la MH et les effets de reprogrammation moléculaire sur la différenciation et l'activité neuronaleFOXO3 is an important transcription factor for stress response, the regulation of differentiation and cell survival that has neuroprotective effects in several models of neurodegenerative diseases, including Huntington’s disease (HD). The neuroprotective effects of FOXO3 in HD are repressed by abnormal signaling from the Wnt receptor Ryk by the binding of the intracellular domain of Ryk to the β-catenin, a cofactor of FOXO3.The aim of this work was to explore the effect of the mutant huntingtin (mHTT) on the repertoire of direct FOXO3 targets (F3Ts) using a model of developmental stage of HD, namely HD isogenic neural stem cells derived from Huntington’s Induced Pluripotent Stem cells. Forming a tripartite complex with β-catenin and FOXO3, Ryk acts as a co-regulator of FOXO3 in normal or pathological condition. Analysis of direct FOXO3 targets shows reprogramming of these targets with losses and gains in signaling pathways that are known to role in HD, including regulatory pathways of cell proliferation. These results show that gene regulation by FOXO3 is heavily modified in cells expressing the mutant huntingtin. Our findings open the way for a comprehensive study of cellular homeostasis mechanisms under the control of FOXO3 in neural differentiation and their impact on the activity of adult neurons. More broadly, these results provide insight into the molecular dynamics of MH and the effects of molecular reprogramming in differentiation and neuronal activity
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Freitas, Ana Maria Salgueiro. "Effects of ataxins-3 loss and gain of function : characterization of neuronal cell lines overexpressing wild-type and mutant forms of mutant ataxin-3." Master's thesis, 2013. http://hdl.handle.net/1822/27817.
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Dissertação de mestrado em Genética MolecularMachado-Joseph Disease (MJD), also known as spinocerebellar ataxia type 3 (SCA3), is an autosomal dominant neurodegenerative disorder which involves the cerebellar, pyramidal, extrapyramidal, motor neuron and oculomotor systems. MJD is caused by an expanded CAG repeat in the coding region of the ataxin-3 gene; for this reason it belongs to the group of polyglutamine (polyQ) associated diseases. The normal function of the ataxin-3 protein (ATXN3) remains mostly unknown, although there are some data suggesting a role for this protein in the modulation of protein degradation (either by the UPS or through autophagy) in association with its deubiquitylase (DUB) activity. Other evidence suggests a role in transcription regulation, in the cellular response(s) to stress and in the cytoskeleton organization as well as in cellular adhesion. In this work we studied the normal function of ATXN3 in neurons, using a novel neuroblastoma SH-SY5Y cell-based approach. We characterized all the different cell lines, assessing cell differentiation and survival, morphology, adhesion and cytoskeleton features, in cells overexpressing wild-type (ATXN3_28Q) and expanded (ATXN3_83Q) ATXN3 as well as cells expressing a catalytic mutant version of this protein (ATXN3_C14A). We also evaluated the transcriptomic profile and protein expression of the cell lines and further investigated the pathways underlying the cellular changes and cytoskeletal regulators. Moreover, in cells expressing both mutant and expanded ATXN3, we found a decreased expression of α-5 integrin (ITGA5) and inhibition of its downstream partners’ activity. The findings described in this study led us to hypothesize that the DUB activity of ATXN3 underlie the neuronal phenotype regulation and also that the expansion of the polyQ tract causes partial loss of function.
A doença de Machado-Joseph (DMJ), também conhecida como ataxia espinocerebelar 3, é uma desordem autossómica dominante que envolve os sistemas cerebelar, piramidal, extrapiramidal, motor neuronal e oculomotor. A DMJ é causada por uma expansão no codão CAG na região codificante do gene da ataxina-3; por esta razão, pertence ao grupo das doenças associadas às poliglutaminas (poliQ). A função normal da proteína ataxina-3 permanece desconhecida, embora alguns dados sugiram um papel da modulação da degradação proteica (quer pelo UPS ou por autofagia) em associação com a sua actividade como deubiquitilase (DUB). Outras evidências apontam para funções relacionadas com regulação da transcrição, como resposta celular ao stress, no citoesqueleto e adesão celular. Neste trabalho estudámos a função normal da ATXN3 em neurónios, usando uma nova abordagem com uma linha neuronal SY5Y de neuroblastoma. Caracterizámos as diferentes linhas celulares, nomeadamente diferenciação celular e sobrevida, morfologia, propriedades de adesão e citoesqueleto em células sobreexpressando a estirpe selvagem da ATXN3 (ATXN3_28Q), a forma expandida (ATXN3_83Q) assim como células sobre-expressando uma versão catalítica mutante (ATXN3_C14A) desta proteína. Avaliámos as diferenças na expressão transcripcional e proteica entre as linhas celulares e investigámos quais as vias de sinalização envolvidas nas alterações celulares observadas e reguladores do citoesqueleto. As células sobre-expressando ambas as formas mutante e expandida, da proteína apresentaram uma expressão diminuída da α5 integrina (ITGA5) bem como uma inibição da actividade desta proteína ao longo da via. As evidências resultantes deste estudo levaram-nos a colocar a hipótese que a actividade DUB da ATXN3 está na base da regulação do fenótipo neuronal e também que a expansão do tracto de poliglutaminas causa uma perda parcial da função da ataxina-3.
Books on the topic "Neuronal cell loss"
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Soileau, Michael J., and Kelvin L. Chou. Parkinson Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0002.
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Parkinson disease is a neurodegenerative disorder characterized clinically by tremor, rigidity, bradykinesia, and postural instability and pathologically by loss of nigrostriatal neurons and deposition of alpha-synuclein in neuronal cell bodies and neuritis. Non-motor symptoms such as psychiatric disorders, cognitive abnormalities, sleep dysfunction, autonomic dysfunction, and sensory manifestations are also common. This chapter gives a broad overview of this disorder. Sections cover pathophysiology, genetics, clinical manifestations, and disease course. The chapter also briefly discusses how to make the diagnosis, and alternative conditions that should be considered.
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Lees, A. J. Parkinson’s disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0008.
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The following landmark discoveries in our understanding of Parkinson’s disease are considered in this chapter: the first full medical description of the malady; consistent severe loss of pigmented cells in the substantia nigra; severe depletion of striatal dopamine; the use of high doses of racemic dopa to improve the motor symptoms; a superior animal model for the study of potential new treatments; functional lesioning and deep brain stimulation to relieve symptoms; capability of fetal dopamine cells to reinnervate the striatum and improve handicap; a compensatory phase before the emergence of motor symptoms and nigral cell loss beginning about five years prior to the onset of presenting symptoms; a large autosomal dominant family with Parkinsonism found to carry a genetic mutation of alpha synuclein; and discovery of Lewy bodies in surviving grafted fetal neuronal cells many years after successful implantation.
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Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.
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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
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Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.
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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
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Fink, John K. Upper Motor Neuron Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0031.
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Symptomatic disturbance of corticospinal and corticobulbar tracts (collectively, the upper motor neuron UMN) occurs in innumerable acquired central nervous system disorders including the consequences of trauma, hypoxia-ischemia, inflammation (e.g. multiple sclerosis), toxins (e.g. thiocyanate1 and specific organophosphorus compound toxicity2) and deficiencies (e.g. hypocupremia3 and vitamin B12 deficiency). Variable degrees of UMN disturbance frequently accompany degenerative disorders in which disturbance of another neurologic system results in the primary clinical. Neuropathologic studies have shown prominent axon degeneration involving corticospinal tracts (HSP and PLS) and corticobulbar tracts (PLS); and mildly affecting dorsal columns (HSP and PLS to some degree). Myelin loss is considered secondary to axon degeneration. Loss of cortical motor neurons is observed in PLS. Anterior horn cells are typically spared in both HSP and PLS. Presently, treatment for HSP and PLS is symptomatic and includes physical therapy and spasticity reducing medications.
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Ferraiuolo, Laura, and Stephen J. Kolb. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0026.
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An overriding mystery of ALS pathogenesis orbits around the molecular basis of selective motor neuron vulnerability and clouds our view. There are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Motor neuron vulnerability is likely related to the unique biological characteristics of these cells. This chapter introduces central molecular pathways that appear to be involved in the pathogenesis of ALS, and highlights why dysregulation of these mechanisms could lead to motor neuron death. Indeed, there are likely mechanisms involved in the initiation of motor neuron loss and mechanisms involved in the progression of motor neuron loss once initiated. Our task is to determine those mechanisms that are relevant to ALS pathogenesis that may be targeted therapeutically to prevent onset and/or halt progression.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
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Ehrlich, Benjamin. The Dreams of Santiago Ramón y Cajal. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190619619.001.0001.
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This book contains the first English translation of the lost dream diary of Santiago Ramón y Cajal (1852–1934), the Nobel Prize-winning “father of modern neuroscience.” In the late nineteenth century, while scientific psychologists searched the inner world of human beings for suitable objects of study, Cajal discovered that the nervous system, including the brain, is composed of distinctly independent cells, later termed neurons. “The mysterious butterflies of the soul,” he romantically called them, “whose beating of wings may one day reveal to us the secrets of the mind.” Cajal was contemporary with Sigmund Freud (1856–1939), whose “secrets of the mind” radically influenced a century of thought. Although the two men never met, their lives and works were intimately related, and each is identified with the foundation of a modern intellectual discipline—neurobiology and psychoanalysis—still in conversation and conflict today. In personal letters, Cajal insulted Freud and dismissed his theories as lies. In order to disprove his rival, Cajal returned to an old research project and started recording his own dreams. For the last five years of his life, he abandoned his own neurobiological research and concentrated on psychological manuscripts, including a new “dream book.” Although his intention was to publish, the project was never released. The unfinished work was thought to be lost, until recently, when a Spanish book appeared claiming to feature the dreams of Cajal, along with the untold story of their complex journey into print.
Book chapters on the topic "Neuronal cell loss"
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Liberman, M. Charles. "Noise-Induced Hearing Loss: Permanent Versus Temporary Threshold Shifts and the Effects of Hair Cell Versus Neuronal Degeneration." In The Effects of Noise on Aquatic Life II, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2981-8_1.
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Lopez-Gutierrez, Javier, and B. Mario Cervantes. "Achalasia." In Mastering Endo-Laparoscopic and Thoracoscopic Surgery, 201–6. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3755-2_31.
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AbstractAchalasia is the result of a progressive degeneration process of the ganglion cells of the myenteric plexus, located in the esophageal wall. The disorder motility that characterizes achalasia appears to result primarily from the loss of inhibitory neurons within the wall of the esophagus itself. This loss of the inhibitory innervation in the LOS causes the basal sphincter pressure to rise and renders the sphincter muscle incapable of normal relaxation. The loss of inhibitory neurons from the smooth muscle portion of the esophageal body results in aperistalais [1]. The manifestations of the disease depend on the degree and location of ganglion cell loss [2]. Loss of peristalsis in the distal esophagus and LOS failure to relax with swallowing, both impair esophageal emptying. Most of the signs and symptoms of achalasia are due to the defect in LES relaxation. Esophagogastric junction (OGJ) outflow obstruction. The risk of developing esophageal cancer increases up to 3.3% after a mean symptom duration of 13 years [3].
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Nitsch, C., B. Eiche, J. Ulrich, and D. Monard. "On the Role of Glia-Derived Protease Nexin-1 in Neuronal and Glial Adaptation to Ischemia-Induced Cell Loss in Human Brain." In Maturation Phenomenon in Cerebral Ischemia II, 151–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60546-8_19.
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Yadav, Divyansh, and Seema Nara. "Nanozymes for Neurodegenerative Diseases." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 77–95. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_9.
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AbstractNeurodegenerative diseases are incurable diseases that get worse as time passes. These diseases are very heterogeneous in nature but have common characteristics like abnormal deposition of protein, glycation, inflammation in particular areas of the brain, and progressive neuronal loss due to oxidative stress. Among these, oxidative stress alone causes a high level of degeneration of neurons. To reduce oxidative stress, natural antioxidants are used but they have some drawbacks like instability, high cost and low reusability. To overcome this, nanozymes are introduced and we have emphasized on major nanozymes whose antioxidant capability has been proven which are gold nanozymes, fullerene, nanoceria, and quantum dots. Gold nanoparticles and their conjugates with other molecules can mimic the enzymatic activity of superoxide dismutase and catalase which decrease the amount of hydrogen peroxide and superoxide radicals in cells. Gold Nanozyme treatment reduces the oxidative stress, nitrite, and sulfhydryl levels in the brain and also rectifies the superoxide dismutase, glutathione, and catalase activity levels. Fullerenols has shown superoxide dismutase activity which was 268 times more effective than mannitol and 37 times more effective than Vitamin E for lipid radicals. Nanoceria has the ability to mimic Superoxide Dismutase as well as catalase activity, can also detoxify peroxynitrite. Quantum dots (QDs) like Graphene Oxide QDs can scavenge the reactive oxygen species and also show indirect activity which alleviates the pathogenesis of the disease. Thus, a nanozyme can be used as an efficient nanomedicine if it is tailored to possess high catalytic activity while eliminating all complications.
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Swaab, D. F., E. Fliers, and E. Goudsmit. "Differential Cell Loss in (Peptide) Neurons in the Anterior Hypothalamus with Aging and Alzheimer’s Disease: Lack of Changes in Cell Density." In Neurology, 119–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70007-1_14.
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Rubin, Devon I. "Basics of Neurophysiology." In Clinical Neurophysiology, edited by Devon I. Rubin, C1—C1.P35. 5th ed. Oxford University PressNew York, 2021. http://dx.doi.org/10.1093/med/9780190067854.003.0002.
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Abstract The physiology of resting membrane potentials, action potentials, and transmission of the electrical signals along neurons and between different cells forms the basis of clinical neurophysiology. The transmission of information in the nervous system depends on the generation of a resting potential through variable permeability of ions across cell membranes controlled by the ionic concentration gradients. Propagated action potentials arise when local potentials reach threshold, allowing for information to move from one area to another within the nervous system. The information is integrated in neurons by the interaction of local potentials generated in response to the neurotransmitters released from depolarized nerve terminals. In this system, information can be coded either as the rate of discharge in individual cells or axons or as the number and combination of active cells. While the physiology and activity of the nervous system can be described in terms of the electrical activity of single cells, the combined activity of large numbers of cells and axons determines the behavior of the organism. Each type of alteration in neuronal or muscle cell physiology can produce symptoms. The particular findings in a patient depend on which cells are altered and the length of alteration. These may include loss or abnormal sensory symptoms, such as tingling or visual obscurations, loss of strength, decrease in consciousness, or abnormal movements. These physiological alterations are not specific and may be the result of many different pathologic mechanisms and diseases. This chapter reviews the basic principles underlying the activity of excitable cells as they apply to the basic neurophysiology of neurons and myocytes.
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D. Udovin, Lucas, Andrea Aguilar, Tamara Kobiec, María I. Herrera, Santiago Perez Lloret, Nicolás Toro Urrego, and Rodolfo A. Kölliker Frers. "Neuroprotective Properties of Cannabinoids in Cellular and Animal Models: Hypotheses and Facts." In Neuroprotection - New Approaches and Prospects. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90761.
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Progressive neuronal loss is a typical characteristic of neurodegenerative diseases. In Parkinson’s disease, the loss of dopaminergic neurons in the basal ganglia results in impaired mobility and flawed muscle control. The loss of cholinergic neurons largely in the basal forebrain contributes to memory and attention deficits and the overall cognitive impairment in Alzheimer’s disease. This being said, neuroprotective drugs should be expected to preserve and/or restore the functions affected by neuronal loss, and substantially prevent cell death. The endocannabinoid system, comprising lipid mediators able to bind to and activate cannabinoid receptors, has emerged as a therapeutic target of potential interest in a variety of central nervous system diseases. Palmitoylethanolamide (PEA) is one of the most important endocannabinoids, which has a key role in modulating oxidative stress and inflammatory response with neuroprotective potential in neurological disorders. Neurodegenerative diseases undergo varied, progressive stages. The current therapeutical approaches are beginning to fall short when it comes to meet the expected results, urging to either develop or identify or develop new effective treatments. This chapter discusses the neuroprotective potential of new drugs, aiming to shed some light on their proposed mechanism of action and their effect in cellular and animal models of neurodegeneration.
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Howard, Gary C. "Death of Cells." In The Biology of Death, 131–51. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190687724.003.0008.
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Many cells have a normal life span, after which they simply wear out, die, and are discarded. These include skin cells, the cells that line the intestines, and blood cells. When things go wrong, cells in other organs die, but the entire organism does not necessarily die. For example, cell death in the brain or heart is serious because those organs have only a limited ability to regenerate. Alzheimer’s disease and Parkinson’s disease involve a breakdown of the neuronal network and loss of specific neurons. Death shapes individual organisms during development. The best-known example is in insects. Caterpillars undergo metamorphosis to become butterflies. Under certain disease conditions, cells “commit suicide” by turning on pathways that lead to death. Those mechanisms include apoptosis, autophagy, necrosis, and necroptosis. In recent years, there has been considerable research into ways that these pathways might be manipulated therapeutically.
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Foster, Paul J., Anthony Khawaja, Lisanne J. Balk, Zaynah Muthy, and Axel Petzold. "Sensory loss—vision." In Oxford Textbook of Neurologic and Neuropsychiatric Epidemiology, edited by Carol Brayne, Valery L. Feigin, Lenore J. Launer, and Giancarlo Logroscino, 345–54. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198749493.003.0033.
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This chapter focuses on degenerative optic neuropathy. The retina and optic nerve share their embryological origin with the brain and are widely regarded as part of the central nervous system. Retinal microvasculature and neuronal components offer a unique ‘window’ on tissues that are closely allied to intracranial structures. Consequently, the eye is vulnerable to the same processes that cause neurodegenerative diseases. Axonal damage in the brain may affect the retinal nerve fibre layer (RNFL), the inner plexiform, and ganglion cell layers, halting at the level of the inner nuclear layer. On this basis, it seems that it is likely that patterns and trends in the inner retinal layers mirror those in the brain, and that these patterns may reflect wider risk of neurodegenerative changes. The dementias and Parkinson’s disease are associated with measurable changes in the retina and optic nerve. Two specific forms of degenerative optic neuropathy that deserve special consideration on the basis of their greater frequency are glaucoma and multiple sclerosis (MS) associated optic neuritis (MSON).
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Schaible, Hans-Georg, and Rainer H. Straub. "Pain neurophysiology." In Oxford Textbook of Rheumatology, 431–36. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059_update_002.
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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
Conference papers on the topic "Neuronal cell loss"
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Cao, Guoxin, You Zhou, Jeong Soon Lee, Jung Yul Lim, and Namas Chandra. "Mechanical Model of Neuronal Function Loss." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-39447.
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The mechanism of mild traumatic brain injury (mTBI) is directly related to the relationship between the mechanical response of neurons and their biological/chemical functions since the neuron is the main functional component of brain.1 The hypotheses is that the external mechanical load will firstly cause the mechanical deformation of neurons, and then, when the mechanical deformation of neurons reaches to a critical point (the mechanical deformation threshold), it will initiate the chemical/biological response (e.g. neuronal function loss). Therefore, defining and measuring the mechanical deformation threshold for the neuronal cell injury is an important first step to understand the mechanism of mTBI. Typically, the mechanical response of neurons is investigated based on the deformation of in vitro model, in which the neurons are cultured on the elastic substrate (e.g. PDMS membranes). The elastic membrane is deformed by the external load, e.g. equibiaxial stretching. The substrate deformation is considered to be the deformation of neurons since the substrate is several orders stiffer than the neurons and the neurons are perfectly bonded with the substrate. The fluoresce method is typically used to test the cell injury, e.g. the cell vitality and the neuron internal ROS level.1, 2
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Park, Sunghee E., Kang-Il Song, Jun-Kyo F. Suh, and Inchan Youn. "Characteristics of the neuronal firing patterns in the subthalamic nucleus with graded dopaminergic cell loss in the nigrostriatal pathway." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7318902.
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Valdes, Alberto, Alejandro Cifuentes, Jose David Sanchez-Martinez, Miguel Herrero, Rocio Gallego, and Zully Suarez-Montenegro. "Foodomics study of the neuroprotective potential of natural products." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/bdyo8801.
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Worldwide, around 50 million people have dementia with nearly 10 million new cases every year. Alzheimer’s Disease (AD) is the most common form of dementia, and it may contribute to 60–70 % of these cases. This multifactorial pathophysiology has been widely characterized by neuroinflammation, extensive oxidative damage, synaptic loss and neuronal cell death. However, only a few drugs have been approved for the therapeutic treatment of AD (with unpleasant side effects), and many studies have suggested that diet and/or food components can prevent the onset of AD. Among these constituents, terpenoids and carotenoids from diverse natural sources have been investigated, and based on a Foodomics approach, our group has demonstrated that an olive leaves extract enriched in triterpenoids and a carotenoids-enriched extract from Dunaliella salina microalgae have neuroprotective potential using in vitro assays. In addition, the neuroprotective and anti-inflammatory potential of these extracts have been confirmed in a neuronal in vitro cell culture model and in vivo using a transgenic Caenorhabditis elegans model. Moreover, different lipidomics studies were performed using advanced analytical methodologies, namely, charged-surface hybrid chromatography-quadrupole-time of flight mass spectrometry (CSH-Q-TOF MS/MS). This technology allowed the annotation of more than 250 intracellular lipids, and among them, a number of phosphatidylcholines, phosphatidylethanolamines and triacylglycerols were significantly altered, suggesting triterpenoids from olive leaves and carotenoids from microalgae as good neuroprotective candidates.
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Guelli, Mariana Sandoval Terra Campos, Daniela Bastos de Almeida Zampier, Lorena Araújo Silva Dias, and Marina de Oliveira Nunes Ibrahim. "Creutzfeldt-Jakob Disease - a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.126.
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Background: Creutzfeldt-Jakob disease (CJD) is a progressive, rare, fatal and rapid human neurodegenerative disease that occurs in the etiologies: sporadic (CJD), familial, iatrogenic (CJD) and CJD variant (CJV) in which cell prion protein (PrP) can be transmitted through animals. Objectives: Literature review about Creutzfeldt-Jakob diseaseDesign and setting: Literature review development in the Centro Universitário de Volta Redonda, Rio de Janeiro, Brazil. Methods: The Creutzfeldt-Jakob disease, infectious diseases and neuroinfection indexes were used in the PUBMED and Scielo databases. Results:CJD has different etiologies with different clinical and pathological phenotypes. CJDV shows psychiatric behaviors and symptoms followed by abnormalities, ataxia and dementia. The sporadic form is the most common, with a progressive clinical course with generalized brain deposition of abnormal prion protein aggregates (PrPTSE) that leads to spongiform change, gliosis and neuronal loss. CJD progresses to dementia and two or more symptoms: cerebellar or visual impairments; pyramidal or extrapyramidal signs; myoclonus; and akinetic mutism. Complex periods of acute wave in the electroencephalogram (EEG) are strongly suggestive of prionic diseases. Rapidly evolving field neuroimmune disorders have shown an increasing in autoantibody testing; attempt to diagnose a range of immune-mediated conditions. Evidence indicates that diffusion-weighted magnetic resonance imaging (DWI) is more sensitive for detecting signal abnormalities. Conclusion: The disease progresses to dementia, accompanied by myoclonus, pyramidal signs and characteristic EEG. It is a complex pathology, which has only symptomatic treatment and requires strict control of reservoirs and risk of contamination.
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Silva, Gustavo Figueiredo da, Caroline Figueiredo da Silva, Washigton Luiz Gomes de Medeiros Junior, and Marcus Vinícius Magno Gonçalves. "Anti -Iglon5 Syndrome: What we know so far? A non-systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.237.
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Background: The first report of Anti-IgLON5 syndrome was in 2014. AntiIgLON5 antibodies have a prevalence of 12 in 150,000 patients per year. However, considering the unreported patients, the prevalence can be much higher. Objectives: Provide an overview of the current knowledge of Anti- IgLON5 syndrome. Design and setting: Narrative review. Methods: Non- systematic review on Pubmed database. Results: The IgLON proteins are a family of cell adhesion molecules and the presence of antibodies against IgLON5 is crucial for the AntiIgLON5 Syndrome diagnosis. This syndrome has an expanded clinical spectrum that involves prominent sleep disorder, progressive bulbar dysfunction, gait instability with abnormal eye movements reminiscent, and cognitive deterioration sometimes associated with chorea. The main neuropathological finding is the neuronal loss with hyperphosphorylated tau protein accumulation at the hypothalamus, brainstem tegmentum, hippocampus, periaqueductal gray matter, medulla oblongata, and upper cervical cord. The exact pathogenesis is still unclear and involves a neurodegenerative process and autoimmune response. Early diagnosis is important to avoid unnecessary tests and prevent complications. Important resources for diagnosis are the antibody testing of serum and cerebrospinal fluid for IgLON5-IgG. The Anti-IgLON5 syndrome mortality is high and new studies published described a good response to immune therapy, however, depends on some clinical and analytical characteristics. Conclusions: The Anti-Iglon5 syndrome is a pathology still poorly studied and described in the medical literature (only in case series, for example), being a syndrome probably underdiagnosed. Future studies are needed to thoroughly analyze the aspects of pathogenesis and treatment of this important pathological syndrome.
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Lee, Sung Jin, Jingjing Sun, Michael King, Huikai Xie, and Malisa Sarntinoranont. "Viscoelastic Property Changes of Acute Rat Brain Tissue Slices as a Function of Cell Viability." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53909.
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Changes in mechanical properties within brain tissues after losses in cell viability have not been well investigated. Lack of oxygen and nutrient transport can induce hypoxic neuronal injury and increase cell membrane permeability, and cell membranes and matrix components can lose their structural and mechanical integrity. These physical changes may have an effect on mechanical properties of brain tissue [1]. In this study, the viscoelastic behavior of two anatomical regions (cerebral cortex and hippocampus) in acute rat brain tissue slices were measured as a function of cell viability using indentation combined with optical coherence tomography (OCT). Neuronal viability in brain tissue slices was determined by measuring Fluoro-Jade C (FJC) staining to assay neuronal death or degeneration as a function of incubation time. OCT-measured deformation depths were compared with finite element (FE) simulations to estimate the relaxation of shear modulus. Measured equilibrium shear modulus (μ∞) after 8 hrs incubation was lower than μ∞ measured after 2 hrs incubation in the cerebral cortex (μ∞, 2hrs = 225 Pa, μ∞, 8hrs = 62 Pa) and hippocampus regions (μ∞, 2hrs = 170 Pa, μ∞, 8hrs = 33 Pa). Instantaneous shear modulus (μ0) after 8 hrs incubation was also an order of magnitude lower than μ0 after 2 hrs incubation in cortex (μ0, 2hrs = 1600 Pa, μ0, 8hrs = 100 Pa) and hippocampus regions (μ0, 2hrs = 370 Pa, μ0, 8hrs = 70 Pa). The results of this study provide a timeline for measuring mechanical properties of brain tissues ex vivo and provide better understanding of changes in brain modulus after injury or cell death.
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Araldi, Bianca Barbosa, Victor Hugo Gomes, Bruno Ludvig Vieira, Klesia Adayani Rodrigues, Andressa Gabrieli da Silva, Leticia Scolari, Gabriela Vasconcellos Santana, Jessica Marafiga, Maria Paula Carvalho, and Heloise Helena Siqueira. "Effects of multiple sclerosis in pregnant and post-birth: particularities of the disease activity." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.704.
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Introduction: Demyelinating diseases are a heterogeneous group of neurological diseases related to autoimmunity whose representative is Multiple Sclerosis (MS). It is characterized by an immune-mediated demyelination of the central nervous system, with a typical outbreak and remission clinic. During pregnancy, a reduction in disease activity was noted due to immunomodulatory effects, and an increase in outbreaks in the puerperium. Thus, our goal is to demonstrate the relationship between pregnancy and MS. Methods: This is a systematic bibliographic review based on searching the SCIELO, PUBMED and UPTODATE databases using the words “Multiple Sclerosis”, “Pregnancy”, “Demyelinating diseases” and “Neurological Disorders”. Discussion: Pregnancy is responsible for numerous changes in the maternal body resulting from hormonal changes with an immunological and neuroprotective effect. Until the beginning of the 20th century, it was considered a risk factor or precipitator of outbreaks in these patients. In 1950, Tillmann et al. questioned him and concluded that pregnancy reduces the risk of outbreaks of the disease and that relapses were more associated with postpartum. The question is still raised by several authors, due to their interest in the search for intricate protective factors in the genesis and cure of the disease. It is believed that immunological changes in pregnancy tend to suppress the maternal immune system preventing fetal rejection, and together with gestational hormones, they are able to make neuronal tissue more resistant to inflammatory aggression and greater capacity for cell repair. In the puerperium, there was an increase in outbreaks of the disease, probably associated with a reduction in hormone levels, the effects of which are lost after the elimination of the fetus. Breastfeeding is not associated with the prevention or risk of new MS outbreaks. The frequency of outbreaks before conception is the only independent predictor of new post-term episodes. There is no consensus regarding the therapeutic approach in these pregnant women. Conclusion: Evidence supports the association between pregnancy, reduced activity of MS and increased activity in the 3 months postpartum, due to the probable loss of neuroprotective effects associated with hormones. Recommendations regarding the use of immunomodulator are suspended before conception (“washout”) until term. New evidence did not associate the use of interferon-β with abortion, cesarean section or low birth weight. There was a benefit of long-term parity with a cumulative effect on the patient’s immunohumor modulation.
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Omar, Hamzeh W., and Harini G. Sundararaghavan. "Effects of Cytoskeletal Tension on Chick Dorsal Root Ganglia." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14585.
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About 50,000 cases of peripheral nerve injuries occur annually [1] resulting in patient pain or loss of touch. Methods of repairing peripheral nerve gaps is essential for aiding in patient recovery. During development, growth, and joint movement, nerves are exposed to mechanical tension that is hypothesized to aid in their growth. Neurons can grow less than .5–1 mm/day but are known to grow up to ∼3 cm/day during development, theorized from factors of stretch on cell cytoskeleton during growth [2,3]. Our focus was to investigate the effects of mechanical strain on nerve growth. We fabricated biodegradable, electrospun, polycaprolactone (PCL) scaffolds to create three-dimensional, nanofibrous networks for Dorsal Root Ganglia (DRG) neuron extension and growth. To test the effects of scaffold stretch and tension on DRG growth, scaffolds were stretched using a custom scaffold stretcher. DRG growth was investigated for 3mm changes in scaffold length on days 0 and 1 of DRG development. Further investigation of DRG growth on day 2 and 3 as well as stretches of 6 and 9mm are being performed. In addition, an incremental stretch test for total stretches of 3, 6, and 9mm will be performed.
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Vandaele, Mathieu, Bryan S. Joyce, and Pablo A. Tarazaga. "Design and Characterization of Piezo-Based Stereocilia." In ASME 2013 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/smasis2013-3189.
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The hair cells in the cochlea are responsible for transforming sound-induced vibration into electrical signals. Damage to these hair cells is among the most common forms of hearing loss in the developed world. Researchers have studied various artificial hair cell (AHC) designs for replacing these hair cells. One such method uses piezoelectric beams to mimic the hair cell’s mechanoelectrical transduction. A piezoelectric beam will produce an electric potential from an applied sound pressure. In the literature, the response of the cochlea to sound pressures is often described using tuning curves. Tuning curves plot the sound pressure level at a given frequency which produces a particular displacement, velocity, or neuron firing rate. The work presented here examines using piezoelectric AHC’s to mimic cochlear hair cells by creating tuning curves of constant tip velocity and voltage. A piezoceramic (PZT) beam and a piezo film (PVDF) bending sensor are examined. An output feedback controller based on PID control is developed to vary the sound pressure from a speaker to create tuning curves for the piezoelectric AHC’s. The tuning curves for the piezoelectric beams are compared to measurements obtained from the biological cochlea.
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Gonçalo, Ana Clara Mota, and Kaline dos Santos Kishishita Castro. "Treatment and main complications of Amyotrophic Lateral Sclerosis: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.520.
Full textAbstract:
Background: Greek, the word sklerosis means hardening. In medicine, the term sclerosis refers to the stiffening of body tissues - scars. These scars (sclerosis), when located in motor neurons, are signs of Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that affects neurons located in the primary motor cortex, brain stem, spinal cord and pyramidal tract. ALS has no cure and its treatment options are currently limited. Objectives: Review on the major complications of ALS, as well as the therapeutic methods for its treatment. Methods: Study conducted trough articles found on The New English Journal of Medicine, SpringerLink and Scholar Google and dated between 2009 and 2021. Results: ALS is known for the gradual atrophy of the muscle fibers associated with muscle loss, dysarthria and dysphagia complicated by sialorrhea, depending on the condition. All forms of the disease lead to paralysis, which causes the main consequent complication for the early mortality of patients - respiratory failure. The treatment of ALS has only one specific approved drug: riluzole, which decreases motor neuron damage, reducing disease progression and increasing patient survival. New therapeutic methods are being studied, such as treatment with stem cells and STING- induced inflammation, but they remain with limited evidence. Conclusions: ALS still has extremely restricted targeted treatment. There’s evident need for further studies aimed at a greater understanding of therapies with the potential to become effective in delaying the progression of the disease.
Reports on the topic "Neuronal cell loss"
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Kamaruzzaman, Mohd Amir, Muhammad Hibatullah Romli, Razif Abas, Sharmili Vidyadaran, Mohamad Taufik Hidayat Baharuldin, Muhammad Luqman Nasaruddin, Vishnnumukkala Thirupathirao, et al. Impact of Endocannabinoid Mediated Glial Cells on Cognitive Function in Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0094.
Full textAbstract:
Review question / Objective: This review aims to review systematically, and meta-analyse published pre-clinical research about the mechanism of endocannabinoid system modulation on glial cells and their effects on cognitive function in designated Alzheimer’s Disease (AD) in the animal model. Condition being studied: Its been acknowledged that the cure of Alzheimer's disease is still vague. Current medicine is working on symptoms only but never stop the disease progression due to neuronal loss. In recent years, researches have found that cannabinoid which is derived from cannabis sativa plant and its compounds exert neuroprotective effects in vitro and in vivo. In fact, cognitive improvement has been shown in some clinical studies. Therefore, the knowledge of cannabinoids and its interaction with living physiological environment like glial cells is crucial as immunomodulation to strategize the potential target of this substance. The original articles from related study relating endocannabinoid mediated glial cell were extracted to summarize and meta-analyze its impact and possible mechanism against cognitive decline in AD.