Готові списки джерел за темами / Cholinergic markers

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Добірка наукової літератури з теми "Cholinergic markers"

Автор: Grafiati

Опубліковано: 10 січня 2023

Оновлено: 29 січня 2023

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Статті в журналах з теми "Cholinergic markers"

Bartus, R. T. "Cholinergic Markers in Alzheimer Disease." JAMA: The Journal of the American Medical Association 282, no. 23 (December 15, 1999): 2208–9. http://dx.doi.org/10.1001/jama.282.23.2208.

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Haroutunian, V., M. Davidson, P. D. Kanof, D. P. Perl, P. Powchik, M. Losonczy, J. McCrystal, D. P. Purohit, L. M. Bierer, and K. L. Davis. "Cortical cholinergic markers in schizophrenia." Schizophrenia Research 12, no. 2 (May 1994): 137–44. http://dx.doi.org/10.1016/0920-9964(94)90071-x.

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Massey, Stephen C., Kevin Blankenship, and Stephen L. Mills. "Cholinergic amacrine cells in the rabbit retina accumulate muscimol." Visual Neuroscience 6, no. 2 (February 1991): 113–17. http://dx.doi.org/10.1017/s0952523800010506.

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AbstractThe cholinergic amacrine cells of the rabbit retina form two mosaics placed symmetrically on either side of the inner plexiform layer. Recently, these cells have been reported to contain immunocytochemical markers for GABA. In this paper, we labeled the cholinergic cells with DAPI, then incubated the retina in [3H]-muscimol, a neuronal marker for GABA. Subsequently, we converted the DAPI fluorescence of the displaced cholinergic matrix to an opaque product by photooxidation in the presence of DAB. Autoradiography showed that all of the displaced cholinergic amacrine cells were labeled with ]3H]-muscimol, thus confirming the immunocytochemical results. The cholinergic cells account for approximately 80% of the cells in the ganglion cell layer which take up ]3H]-muscimol.

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Berger, Michael L., Mario Veitl, Susanne Malessa, Elfriede Sluga, and Oleh Hornykiewicz. "Cholinergic markers in ALS spinal cord." Journal of the Neurological Sciences 108, no. 1 (March 1992): 114–17. http://dx.doi.org/10.1016/0022-510x(92)90196-r.

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Perry, E. K., and R. H. Perry. "CNS cholinergic markers and Alzheimer's disease." Neurobiology of Aging 7, no. 5 (September 1986): 390–91. http://dx.doi.org/10.1016/0197-4580(86)90167-3.

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Reale, Marcella, Lucia Velluto, Marta Di Nicola, Chiara D’Angelo, Erica Costantini, Michele Marchioni, Gianluigi Cerroni, and Biancamaria Guarnieri. "Cholinergic Markers and Cytokines in OSA Patients." International Journal of Molecular Sciences 21, no. 9 (May 5, 2020): 3264. http://dx.doi.org/10.3390/ijms21093264.

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The role of inflammation and dysfunction of the cholinergic system in obstructive sleep apnea (OSA) has not exhaustively clarified. Thus, in this study, we explore the non-neuronal cholinergic system and the balance of T helper (Th) 17- and T regulatory (Treg)-related cytokines in OSA patients. The study includes 33 subjects with obstructive sleep apnea and 10 healthy controls (HC). The expression levels of cholinergic system component, RAR-related orphan receptor (RORc), transcription factor forkhead box protein 3 (Foxp3) and cytokines were evaluated. Th17- and Treg-related cytokines, choline levels and acetylcholinesterase (AChE), butyrylcholinesterase (BuChE) activity were quantified in OSA and control subjects. AChE and nicotinic receptor α 7 subunit (α7nAChR) gene expression and serum levels of choline, AChE and BuChE were lower in OSA patients than in the HC group. Compared with the HC group, OSA patients exhibited an increased expression, secretion and serum levels of pro-inflammatory cytokines, a reduced expression, secretion and serum levels of transforming growth factor (TGF)β and reduced Foxp3 mRNA levels. The Th17/Treg-related cytokine ratio was higher in the OSA group. Our results confirm and reinforce the hypothesis that OSA may be considered a systemic inflammatory disease, and that an imbalance of non-neuronal cholinergic and pro/anti-inflammatory cytokines may contribute to development and progression of comorbidities in OSA subjects. The evaluation of Th17/Treg-related cytokine may provide an additional explanation for OSA pathogenesis and clinical features, opening new directions for the OSA management.

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Volgin, Denys V., Irma Rukhadze, and Leszek Kubin. "Hypoglossal premotor neurons of the intermediate medullary reticular region express cholinergic markers." Journal of Applied Physiology 105, no. 5 (November 2008): 1576–84. http://dx.doi.org/10.1152/japplphysiol.90670.2008.

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The inspiratory drive to hypoglossal (XII) motoneurons originates in the caudal medullary intermediate reticular (IRt) region. This drive is mainly glutamatergic, but little is known about the neurochemical features of IRt XII premotor neurons. Prompted by the evidence that XII motoneuronal activity is controlled by both muscarinic (M) and nicotinic cholinergic inputs and that the IRt region contains cells that express choline acetyltransferase (ChAT), a marker of cholinergic neurons, we investigated whether some IRt XII premotor neurons are cholinergic. In seven rats, we applied single-cell reverse transcription-polymerase chain reaction to acutely dissociated IRt neurons retrogradely labeled from the XII nucleus. We found that over half (21/37) of such neurons expressed mRNA for ChAT and one-third (13/37) also had M2 receptor mRNA. In contrast, among the IRt neurons not retrogradely labeled, only 4 of 29 expressed ChAT mRNA ( P < 0.0008) and only 3 of 29 expressed M2 receptor mRNA ( P < 0.04). The distributions of other cholinergic receptor mRNAs (M1, M3, M4, M5, and nicotinic α4-subunit) did not differ between IRt XII premotor neurons and unlabeled IRt neurons. In an additional three rats with retrograde tracers injected into the XII nucleus and ChAT immunohistochemistry, 5–11% of IRt XII premotor neurons located at, and caudal to, the area postrema were ChAT positive, and 27–48% of ChAT-positive caudal IRt neurons were retrogradely labeled from the XII nucleus. Thus the pre- and postsynaptic cholinergic effects previously described in XII motoneurons may originate, at least in part, in medullary IRt neurons.

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Adem, Abdu, Agneta Nordberg, Gösta Bucht, and Bengt Winblad. "Extraneural cholinergic markers in Alzheimer's and Parkinson's disease." Progress in Neuro-Psychopharmacology and Biological Psychiatry 10, no. 3-5 (January 1986): 247–57. http://dx.doi.org/10.1016/0278-5846(86)90005-9.

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Marinova, Desislava M., Miroslav L. Dobrev, Tihomir R. Rashev, Iskren K. Gerasimov, Vladislav Nankov, and Stefan V. Trifonov. "ACETYLCHOLINE AND ITS SYNTHESIZING ENZYME CHOLINE ACETYLTRANSPHERASE IN THE ENTERIC NERVOUS SYSTEM." Journal of IMAB - Annual Proceeding (Scientific Papers) 28, no. 4 (November 9, 2022): 4671–75. http://dx.doi.org/10.5272/jimab.2022284.4671.

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The enteric nervous system is the largest and most complex division of the peripheral nervous system. Located in the wall of the gastrointestinal tract, it is a regulatory and coordination unit of the nervous system. Neurochemical, pharmacological, and functional studies describe three main classes of neurons in the enteric nervous system– primary afferent, interneurons and motor neurons. These are grouped in ganglia, which are connected and form plexuses. Acetylcholine is a major neurotransmitter that plays a pivotal role in the enteric nervous system and several non-neuronal structures. Internal cholinergic neurons and vagus terminals in the enteric nervous system use acetylcholine as the main excitatory neurotransmitter, regulating motility and mucosal function in the digestive system. The enzyme choline acetyltransferase (ChAT) that catalyzes the synthesis of acetylcholine represents the most specific cholinergic marker. Recent markers used to visualize cholinergic structures are the splicing variants of ChAT mRNA that are transcribed from the ChAT gene. Different alternatively spliced ChAT mRNA variants are transcribed in many animal species, including humans. In the mouse, seven variants in the 5’-noncoding region and two variants that differ in their coding region are described. Morphological, genetic and molecular analysis of ChAT and its splicing variants, as the most reliable and frequently used marker for cholinergic structures, would contribute to a better understanding of the physiological and pathological states of cholinergic neurons in the enteric nervous system.

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Gil-Bea, Francisco Javier, Mónica García-Alloza, Jon Domínguez, Beatriz Marcos, and María Javier Ramírez. "Evaluation of cholinergic markers in Alzheimer's disease and in a model of cholinergic deficit." Neuroscience Letters 375, no. 1 (February 2005): 37–41. http://dx.doi.org/10.1016/j.neulet.2004.10.062.

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Дисертації з теми "Cholinergic markers"

Aubert, Isabelle. "Cholinergic markers in models of neuronal plasticity." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28417.

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Using various markers, the status of brain cholinergic innervation was investigated in different models of neuronal plasticity in which processes of degeneration, regeneration and development are observed. The cholinergic markers evaluated included choline acetyltransferase (ChAT, the synthesizing enzyme of acetylcholine) activity, acetylcholinesterase (AChE, the enzyme which degrades acetylcholine) staining, ($ sp3$H) hemicholinium-3 (HC3, marker of the high-affinity choline uptake system) and ($ sp3$H) AH5183/vesamicol (marker of the acetylcholine vesicular transporter) binding sites. Muscarinic receptors were investigated with ($ sp3$H) QNB (total population of muscarinic sites), ($ sp3$H) 4-DAMP (putative M$ sb1$/M$ sb3$ sites), ($ sp3$H) pirenzepine (putative M$ sb1$ subtype), ($ sp3$H) acetylcholine, ($ sp3$H) AF-DX 116 and ($ sp3$H) AF-DX 384 (putative M$ sb2$ subtype), while ($ sp3$H) N-methylcarbamylcholine and ($ sp3$H) cytisine were used for the nicotinic receptors. These markers were studied (a) in human neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, (b) in entorhinal cortex lesioned rats, a model of plasticity possibly related to the sprouting of the septohippocampal cholinergic pathway, (c) in the aged memory-impaired and memory-unimpaired rats, and finally (d) during the development and maturation of the rat brain from embryogenesis to adulthood.
These markers of the cholinergic synapse are differentially affected depending upon the model studied. In addition, pre- and postsynaptic cholinergic markers are not necessarily altered similarly. For example, muscarinic M$ sb2$ and nicotinic sites decreased in parallel with ChAT activity in the neocortex and hippocampal formation of human brain patients suffering from neurodegenerative disorders such as Alzheimer's or Parkinson's diseases. However, in the aged memory-impaired rats, ChAT activity and nicotinic sites are unaltered while muscarinic M$ sb2$ sites are significantly increased in cortical areas. Moreover, although AChE staining is increased in the hippocampal formation following lesions of the entorhinal cortex, nicotinic binding sites are decreased and other cholinergic markers are unaffected. Finally, during rat brain development, presynaptic markers such as the acetylcholine vesicular transport and nicotinic sites are expressed prenatally, while others like ($ sp3$H) HC3 and muscarinic M$ sb2$ sites appear only postnatally. Muscarinic M$ sb1$ sites are in low amounts prenatally, increasing gradually during postnatal maturation. The distinct ontogenic profile of each cholinergic marker suggests specific roles for the various components of the cholinergic synapse throughout brain development.
Taken together, these results provide information on the differential adaptation, response and possible roles of the various components of the cholinergic synapse in models of neuronal plasticity. For example, nicotinic receptors may play an important role in the development, sprouting and maintenance of a normal cholinergic innervation, while muscarinic M$ sb2$ receptors might contribute to the fine regulation of ACh release, which, if impaired, could produce detrimental effects on cognitive functions such as those seen in the aged memory-impaired rats.

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Fourie, Jeanne. "Age dependent pupillary and cognitive responses to cholinergic drugs as a model for identificaton of future biological markers for Alzheimer's disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq40848.pdf.

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Rathenberg, Jan. "Gene targeting and single-cell electroporation to analyze cholinergic neurons using choline acetyltransferase as marker." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/194/index.html.

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Kuol, Nyanbol. "Interaction Between Immunosuppressive and Cholinergic Markers in Colorectal Cancer." Thesis, 2020. https://vuir.vu.edu.au/42036/.

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Colorectal cancer (CRC) is amongst the leading diagnosed cancers worldwide. Despite the increasing interest to understand, the roles that the nervous and immune systems play in influencing the tumour microenvironment to promote cancer development and progression, more studies are required to understand the mechanism. Cancer cells can influence their microenvironment and bi-directionally communicate with other systems such as the immune and nervous systems. The immune system plays a key role in the eradication of cancer cells. Studies have shown that multiple mechanisms are responsible for the suppression of the immune system in cancer, one of which being the expression of immune checkpoints inhibitors such as programmed death 1 (PD-1), PD-L1, programmed death ligand 1 and 2 (PD-L1, PD- L2), sialic acid-binding lectins 9 (siglec-9) and IDO (indoleamine-2,3-dioxygenase). These molecules function by inhibiting anti-tumour effects of T cell-mediated immune responses. In addition to these molecules, studies have shown that several cancers can release acetylcholine (ACh) and express cholinergic receptors (muscarinic receptor 3 (M3R) and alpha 7 nicotinic receptor (a7nAChR)), overexpress choline acetyltransferase (ChAT), a precursor enzyme required for ACh synthesis and VAChT, essential for transporting of ACh, and excitatory receptor. Currently, there are no data available in determining the interaction between the expression of immunosuppressive and cholinergic markers in cancer, thus, this thesis aims to determine the interaction between the expression of immunosuppressive and cholinergic markers in CRC.

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Rathenberg, Jan [Verfasser]. "Gene targeting and single-cell electroporation to analyze cholinergic neurons using choline acetyltransferase as marker / vorgelegt von Jan Rathenberg." 2002. http://d-nb.info/965461882/34.

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Книги з теми "Cholinergic markers"

Fourie, Jeanne. Age dependent pupillary and cognitive responses to cholinergic drugs as a model for identificaton of future biological markers for Alzheimer's disease. Ottawa: National Library of Canada, 1998.

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Частини книг з теми "Cholinergic markers"

Mash, Deborah C. "Architecture Of Cholinergic Pre-And Postsynaptic Markers In The Primate Striatum." In Progress in Parkinson Research, 31–37. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0759-4_4.

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Downen, Martha, Kimi Sugaya, Stephen P. Arneric, and Ezio Giacobini. "Presynaptic Markers of Cholinergic Function in Cortex Following Ibotenic Acid Lesion of the Basal Forebrain." In Advances in Behavioral Biology, 255–68. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5727-8_22.

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Walch, Christiane, Reinhard Schliebs, and Volker Bigl. "Effect of early visual pattern deprivation on development and laminar distribution of cholinergic markers in rat visual cortex." In Experientia Supplementum, 295–304. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-9138-7_29.

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Jones, D., S. Kelwala, S. Dube, E. Jackson, and N. Sitaram. "Cholinergic Rem Sleep Induction Response as a Marker of Endogenous Depression." In Advances in Behavioral Biology, 375–83. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5194-8_35.

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Nakamura, Shinichi, Hidekazu Tomimoto, Ichiro Akiguchi, and Jun Kimura. "Histochemical Demonstration of Monoamine Oxidase Activity in the Mouse Striatal Cholinergic Neurons and Marked Species Variations among Rodent Striata." In Alzheimer’s and Parkinson’s Diseases, 327–31. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-9145-7_49.

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Giacobini, Ezio, Kiminobu Sugaya, and Rodger J. Elble. "Markers of Cholinergic Dysfunction in Alzheimer Disease." In Alzheimer Disease, 137–56. CRC Press, 2020. http://dx.doi.org/10.1201/9781003067665-12.

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Katzman, Robert, and Katherine Bick. "The Loss of Cholinergic Markers in the AD Brain." In Alzheimer Disease, 179–89. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012401955-3/50013-6.

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Martínez-Murillo, Ricardo, and José Rodrigo. "The Localization of Cholinergic Neurons and Markers in the CNS." In CNS Neurotransmitters and Neuromodulators, 1–37. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068723-1.

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Furey, Maura A., Daniel C. Mathews, and Carlos A. Zarate. "Pathogenesis of Depression: Clinical Studies." In Neurobiology of Mental Illness, edited by Helen S. Mayberg, 438–41. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0033.

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Historically, research focused on themonoaminergicsystemshas contributed to our understanding of theunderlying pathophysiology of affective disorders.Recent directions in clinical and translational research have concentrated on discovering alternative therapeutic targets with the hopes of producing more efficacious and faster-acting antidepressant agents.This chapter offers an overview of recent clinical research targeting the glutamatergic and cholinergic neurotransmitter systems, with particular interest in novel agents that have produced rapid antidepressant effects. Insights into the underlying pathophysiology of mood disorders resulting from this work are reviewed. In addition, the rapidity of clinical response offers the unique opportunity to studybiological markers more efficiently , and to utilize biomarkers to predict treatment outcome. The findings from such studies also are summarized.

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Dorsett, Maia. "Vomiting." In Acute Care Casebook, edited by Jeremy T. Cushman, 47–51. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190865412.003.0011.

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This case illustrates the priorities of management in a patient with acute organophosphate toxicity in the prehospital environment. Organophosphates are common components of pesticides. They act as toxins and can lead to development of the cholinergic toxidrome by blocking breakdown of the neurotransmitter acetylcholine at nerve endings. The cholinergic toxidrome is a clinical syndrome marked by parasympathetic excess (bradycardia, bronchorrhea, bronchospasm, miosis, lacrimation, salivation, urination, and defecation), neuromuscular junction activation (muscle fasciculations), and central nervous system toxicity (delirium and seizures). The priorities of care in organophosphate exposure include rapid administration of antidote (atropine and pralidoxime), airway management, and patient decontamination to prevent further toxin absorption. Medical providers must always protect themselves in the case of toxic exposure and should wear double nitrile gloves at all times when handling the patient or their clothing.

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Тези доповідей конференцій з теми "Cholinergic markers"

Zhi-gang, Mei, Zeng Yong-bao, Liu Xiao-jie, and Wang Ming-zhi. "Efficacy of auricular acupuncture on inflammatory markers and insulin resistance in type 2 diabetes model of rats: In light of cholinergic anti-inflammatory pathway." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6029053.

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Siqueira, Fernando, Vanessa Siqueira, Lucas Falcão, Arthur Bezerra, and Carlos Silva. "THE INFLUENCE BETWEEN ALZHEIMER’S DISEASE AND HEALTHY EATING: A SYSTEMATIC REVIEW." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda062.

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Background: Alzheimer’s Disease (AD) is a neurodegenerative disease responsible for neuronal losses that affect mainly the cortex and hippocampus, which begin to shrink in size, damaging cognitive functions. This process affects cholinergic neurons, influencing acetylcholine (ACH) levels, a memoryrelated neurotransmitter. Glucose metabolism and low thiamine levels appear to be affected by AD. Consequently, diabetes becomes a disease associated with AD and the thiamine deficiency levels depress the use of glucose by the brain. Thus, nutrition may have a role in preventing dementia through the treatment and prevention. Objective: To summarize the knowledge about this topic by reviewing articles and analyzing if healthy eating influences the development of AD. Methods: Selection of articles from the Scielo database. Results: Inflammation contributes to the pathogenesis of AD. The effect observed in patients with adherence to the Mediterranean diet translates into a decrease in inflammatory markers at the plasma level. One of the symptoms, memory loss, can be prevented by a micronutrient named thiamine, a precursor of ACH, it is found in the leguminous. The Mediterranean diet has been shown to attribute a neuroprotective activity which goes with its anti-inflammatory effect. Conclusion: AD starts by its multifactorial etiology that consists of genotype and phenotype. Nutrition would be efficient as a preventive and a therapeutic alternative among other.

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Soares, Izadora Fonseca Zaiden, João Nicoli Ferreira dos Santos, and Lis Gomes Silva. "Dramatic cognitive improvement with acetylcholinesterase inhibitor in cerebral amyloid angiopathyrelated inflammation." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.578.

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Context: Cerebral amyloid angiopathy (CAA) is characterized by progressive deposition of amyloid-ß fibrils in the walls of small arterioles and capillaries of the leptomeninges and cerebral cortex. A rare subtype of CAA is CAA-related inflammation (CAA-RI), which exhibits marked perivascular or transmural inflammatory infiltration in brain tissue. The major clinical features of CAA-RI are rapidly progressive dementia, behavioral changes, headache, seizures, or stroke-like signs. Conclusive diagnosis requires histopathological confirmation, but validated clinicoradiological criteria for the diagnosis of probable CAA-RI have good sensitivity (82%) and specificity (97%). Treatment with high dose corticosteroids with or without other immunosuppressive therapy is recommended. We report a case of probable CAA-RI that did not respond to corticosteroid therapy but had a surprising improvement with acetylcholinesterase inhibitor. Case report: A 77-year-old illiterate woman presented with a history of subacute onset of seizures and behavioral changes. Her medical history was positive for a hearing loss due to a toxic exposure in childhood, and a cured breast cancer. The neurological examination showed attention impairment, disorientation, and incoherent speech. CSF showed a mildly elevated protein count. Brain MRI met criteria for probable CAA-RI. She had a poor response with high doses of corticosteroids, but after a trial with Donepezil she showed important cognitive and functional improvement. Conclusion: This result attracts attention to the importance of the cholinergic pathway in the etiology and pathological mechanisms of CAA. Randomized Controlled Trials would be required to confirm our hypothesis and to find new therapeutic options for CAA.

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Thom, S., A. Hughes, G. Martin, P. Goldberg, and P. Server. "VASODILATOR PEPTIDES - CGRP AND VIP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643720.

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The two peptides calcitonin gene related peptide (C6RP) and vasoactive intestinalpeptide (VIP) are widely distributed in animal species including man and a number ofdiverse actions of the peptides have been described [1,2]. They share vasoactive properties [3,4] and may have important functions as neurotransmitters in a non-adrenergic, non-cholinergic nervous system [5]. VIP has been located in perivascular nerves supplying several tissues and is co-stored with acetylcholine in the parasympathetic system [6]. CGRP has also been widely identified in the nervous system, the cardiovascular system and perivascular nerves, where it is located with substance P[7]. Our studies have assessed the activity of these peptides in a human vascular resistance bed -the forearm, and on isolated human blood vessels.Forearm studies were performed by infusingCGRP (10,30,100 ng/min) or ViP (10,30,100 ng/min) via the brachial artery for 5 min at each dose level and measuring blood flow by venous occlusion plethysmography. In vitro studies were performed using ringsegments of pulmonary, gastric, coronary, radial, and transverse cervical arteries freshly obtained from surgical resection specimens and cerebral arteries obtained from autogsy tissue within 4 hours of death. Vessels were mounted in organ baths containing Krebs buffer aerated with 95% 02, 5% C02 at 37C, and preconstricted using a submaximal concentration of noradrenaline (1-3 μM) or prostaglandin F2a (I-IO11μ7.CGRP or VIP was added to the tissue bath in a cumulative fashion. All arterial segments used for these studies relaxed in response to acetylcholine (0.1-3μM)or A23187 (0.1-3μM) and this was regarded as indicative of functional endothelial integrity. Studies were performed in the presence of indomethacin (lOμM). The endothelium was deliberately removed from some rings and in others haemoglobin (5μM) ormethylene blue (lOμM) were added to the tissue bath after the arterialrings were effectively relaxed by CGRP orVIP. Both peptides produced marked dose dependent increases in forearm blood flow; at 100 ng/min the mean net increase was 174 ± 24% (mean ±s.e.m.) with CGRP, and 223 + 34% (mean +s.e.m.) with VIP. In vitro CGRP (InM-lμM) relaxed preconstricted segments ofradial Tn=2), coronary (n=4), gastric (n=5) and cerebral (n=3) arteries in an endothelium dependent manner. VIP (1 nM - 1pm) also relaxed human gastric (n=2), splenic (n=2), cervical (n=3) and pulmonary (n=5) arteries VIP relaxation of the gastric and cervical arteries was dependent on the presence of endothelium; however, VIP inducedrelaxation of pulmonary artery was not dependent on functional endothelium. The endothelium dependent relaxations could be abolished either by luminal rubbing, additionor haemoglobin or methylene blue. Together these results might be taken to imply that the forearm vasodilatation response is mediated by EDRF. However, caution is necessary in extrapolating from in vitro observations of large vessels to the in vivo response of a resistance vascular bed.Others have demonstrated that the CGRPand VIP relaxatory responses of smaller human pial arteries (ID 250-600 pm) are endothelium independent [8] and preliminary work in our department supports this. The EDRF mechanism is cyclic GMP linked, but most of the studied functions of VIP and CGRP seem to be linked to a rise in cyclic AMP-. A further paradox is that the blood flow response to infused acetylcholine, the archetypal releaser of EDRF, is evanescent, and yet the vasodilator response to CGRP is persistent.

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