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Current Neurovascular Research

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ISSN (Print): 1567-2026
ISSN (Online): 1875-5739

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Perspective Article

The Interplay Among Epilepsy, Parkinson’s Disease and Inflammation: Revisiting the Link through Ca2+/cAMP Signalling

Author(s): Leandro B. Bergantin*

Volume 18, Issue 1, 2021

Published on: 28 June, 2021

Page: [162 - 168] Pages: 7

DOI: 10.2174/1567202618666210603123345

Abstract

Background: Robust evidence has described that Parkinson´s disease (PD) is associated with an increased risk for developing epileptic seizures. In fact, an interplay between PD and epilepsy has been of interest for many years. An emerging hypothesis is that inflammation could link both diseases.

Objective: Bearing in mind the experience of our group in the field of Ca2+/cAMP signalling pathways, this article discussed, beyond inflammation, the role of these signalling pathways in this link between PD and epilepsy.

Methods: Publications involving Ca2+/cAMP signalling pathways, PD, and epilepsy (alone or combined) were collected by searching PubMed and EMBASE.

Results: The comprehension of the interplay between PD and epilepsy could improve the drug therapy. In addition, a Ca2+ signalling dyshomeostasis due to Coronavirus disease 2019 (COVID-19), an emerging and rapidly evolving situation, has been reported.

Conclusion: Thus, this article also debated recent findings about therapeutics involving Ca2+ channel blockers for preventing Ca2+ signalling dyshomeostasis due to COVID-19, including the correlation among COVID-19, epilepsy, and PD.

Keywords: Epilepsy, Parkinson´s disease, Ca2+/cAMP signalling, Ca2+ channel blockers, pharmacotherapy, Coronavirus disease 2019 (COVID-19).

« Previous Next »
[1]
Pajares M, Rojo A, Manda G, Boscá L, Cuadrado A. Inflammation in Parkinson’s disease: Mechanisms and therapeutic implications. Cells 2020; 9(7): 1687.
[http://dx.doi.org/10.3390/cells9071687] [PMID: 32674367]
[2]
Tufekci KU, Meuwissen R, Genc S, Genc K. Inflammation in Parkinson’s disease. Adv Protein Chem Struct Biol 2012; 88: 69-132.
[http://dx.doi.org/10.1016/B978-0-12-398314-5.00004-0] [PMID: 22814707]
[3]
Bergantin LB, Caricati-Neto A. The “Calcium Paradox” and its impact on neurological and psychiatric diseases. Cambridge Scholars Publishing 2018. NLM ID: 101734546
[4]
Vezzani A, Granata T. Brain inflammation in epilepsy: Experimental and clinical evidence. Epilepsia 2005; 46(11): 1724-43.
[http://dx.doi.org/10.1111/j.1528-1167.2005.00298.x] [PMID: 16302852]
[5]
Vezzani A, Baram TZ. New roles for interleukin-1 beta in the mechanisms of epilepsy. Epilepsy Curr 2007; 7(2): 45-50.
[http://dx.doi.org/10.1111/j.1535-7511.2007.00165.x] [PMID: 17505552]
[6]
Riazi K, Galic MA, Pittman QJ. Contributions of peripheral inflammation to seizure susceptibility: Cytokines and brain excitability. Epilepsy Res 2010; 89(1): 34-42.
[http://dx.doi.org/10.1016/j.eplepsyres.2009.09.004] [PMID: 19804959]
[7]
Choi J, Nordli DR Jr, Alden TD, et al. Cellular injury and neuroinflammation in children with chronic intractable epilepsy. J Neuroinflammation 2009; 6: 38.
[http://dx.doi.org/10.1186/1742-2094-6-38] [PMID: 20021679]
[8]
Gruntz K, Bloechliger M, Becker C, et al. Parkinson disease and the risk of epileptic seizures. Ann Neurol 2018; 83(2): 363-74.
[http://dx.doi.org/10.1002/ana.25157] [PMID: 29369409]
[9]
Rana A, Musto AE. The role of inflammation in the development of epilepsy. J Neuroinflammation 2018; 15(1): 144.
[http://dx.doi.org/10.1186/s12974-018-1192-7] [PMID: 29764485]
[10]
Steinlein OK. Calcium signaling and epilepsy. Cell Tissue Res 2014; 357(2): 385-93.
[http://dx.doi.org/10.1007/s00441-014-1849-1] [PMID: 24723228]
[11]
Calì T, Ottolini D, Brini M. Calcium signaling in Parkinson’s disease. Cell Tissue Res 2014; 357(2): 439-54.
[http://dx.doi.org/10.1007/s00441-014-1866-0] [PMID: 24781149]
[12]
Bergantin LB. The interplay between depression and Parkinson’s disease: Learning the link through Ca2+/cAMP signalling. Curr Protein Pept Sci 2020; 21(12): 1223-8.
[http://dx.doi.org/10.2174/1389203721666200206161912] [PMID: 32026774]
[13]
Bergantin LB. Diabetes and Parkinson’s disease: Debating the link through Ca2+/cAMP signalling. Curr Diabetes Rev 2020; 16(3): 238-41.
[http://dx.doi.org/10.2174/1573399815666190711113644] [PMID: 31291877]
[14]
Birbeck GL. Epilepsy care in developing countries: Part I of II. Epilepsy Curr 2010; 10(4): 75-9.
[http://dx.doi.org/10.1111/j.1535-7511.2010.01362.x] [PMID: 20697498]
[15]
Ngugi AK, Bottomley C, Kleinschmidt I, Sander JW, Newton CR. Estimation of the burden of active and life-time epilepsy: A meta-analytic approach. Epilepsia 2010; 51(5): 883-90.
[http://dx.doi.org/10.1111/j.1528-1167.2009.02481.x] [PMID: 20067507]
[16]
Annegers JF, Dubinsky S, Coan SP, Newmark ME, Roht L. The incidence of epilepsy and unprovoked seizures in multiethnic, urban health maintenance organizations. Epilepsia 1999; 40(4): 502-6.
[http://dx.doi.org/10.1111/j.1528-1157.1999.tb00748.x] [PMID: 10219279]
[17]
Hussain SA, Haut SR, Lipton RB, Derby C, Markowitz SY, Shinnar S. Incidence of epilepsy in a racially diverse, community-dwelling, elderly cohort: Results from the Einstein aging study. Epilepsy Res 2006; 71(2-3): 195-205.
[http://dx.doi.org/10.1016/j.eplepsyres.2006.06.018] [PMID: 16870396]
[18]
Joint Epilepsy Council.Epilepsy prevalence, incidence and other statistics. UK and Ireland: Joint Epilepsy Council 2011.
[19]
Salat D, Noyce AJ, Schrag A, Tolosa E. Challenges of modifying disease progression in prediagnostic Parkinson’s disease. Lancet Neurol 2016; 15(6): 637-48.
[http://dx.doi.org/10.1016/S1474-4422(16)00060-0] [PMID: 26993435]
[20]
Hayes MW, Fung VS, Kimber TE, O’Sullivan JD. Current concepts in the management of Parkinson disease. Med J Aust 2010; 192(3): 144-9.
[http://dx.doi.org/10.5694/j.1326-5377.2010.tb03453.x] [PMID: 20121682]
[21]
Braak H, Ghebremedhin E, Rüb U, Bratzke H, Del Tredici K. Stages in the development of Parkinson’s disease-related pathology. Cell Tissue Res 2004; 318(1): 121-34.
[http://dx.doi.org/10.1007/s00441-004-0956-9] [PMID: 15338272]
[22]
Zhang LK, Sun Y, Zeng H, et al. Calcium channel blocker amlodipine besylate therapy is associated with reduced case fatality rate of COVID-19 patients with hypertension. Cell Discov 2020; 6(1): 96.
[http://dx.doi.org/10.1038/s41421-020-00235-0] [PMID: 33349633]
[23]
D’Elia JA, Weinrauch LA. Calcium ion channels: Roles in infection and sepsis mechanisms of calcium channel blocker benefits in immunocompromised patients at risk for infection. Int J Mol Sci 2018; 19(9): 2465.
[http://dx.doi.org/10.3390/ijms19092465] [PMID: 30134544]
[24]
Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet 2020; 395(10229): 1054-62.
[http://dx.doi.org/10.1016/S0140-6736(20)30566-3] [PMID: 32171076]
[25]
Silva IVG, de Figueiredo RC, Rios DRA. Effect of different classes of antihypertensive drugs on endothelial function and inflammation. Int J Mol Sci 2019; 20(14): 3458.
[http://dx.doi.org/10.3390/ijms20143458] [PMID: 31337127]
[26]
Asadi-Pooya AA. Seizures associated with coronavirus infections. Seizure 2020; 79: 49-52.
[http://dx.doi.org/10.1016/j.seizure.2020.05.005] [PMID: 32416567]
[27]
Asadi-Pooya AA, Attar A, Moghadami M, Karimzadeh I. Management of COVID-19 in people with epilepsy: Drug considerations. Neurol Sci 2020; 41(8): 2005-11.
[http://dx.doi.org/10.1007/s10072-020-04549-5] [PMID: 32594268]
[28]
Sulzer D, Antonini A, Leta V, et al. COVID-19 and possible links with Parkinson’s disease and parkinsonism: From bench to bedside. NPJ Parkinsons Dis 2020; 6: 18.
[http://dx.doi.org/10.1038/s41531-020-00123-0] [PMID: 32885037]
[29]
Ribeiro CM. The role of intracellular calcium signals in inflammatory responses of polarised cystic fibrosis human airway epithelia. Drugs R D 2006; 7(1): 17-31.
[http://dx.doi.org/10.2165/00126839-200607010-00002] [PMID: 16620134]
[30]
Dalal PJ, Muller WA, Sullivan DP. Endothelial cell calcium signaling during barrier function and inflammation. Am J Pathol 2020; 190(3): 535-42.
[http://dx.doi.org/10.1016/j.ajpath.2019.11.004] [PMID: 31866349]
[31]
Campbell IL, Abraham CR, Masliah E, et al. Neurologic disease induced in transgenic mice by cerebral overexpression of interleukin 6. Proc Natl Acad Sci USA 1993; 90(21): 10061-5.
[http://dx.doi.org/10.1073/pnas.90.21.10061] [PMID: 7694279]
[32]
Ravizza T, Balosso S, Aronica E, Vezzani A. Epilepsy: Mechanisms, models, and translational perpsectives. Boca Raton: CRC Press 2010; pp. 45-59.
[http://dx.doi.org/10.1201/9781420085594-c4]
[33]
Vezzani A, Moneta D, Conti M, et al. Powerful anticonvulsant action of IL-1 receptor antagonist on intracerebral injection and astrocytic overexpression in mice. Proc Natl Acad Sci USA 2000; 97(21): 11534-9.
[http://dx.doi.org/10.1073/pnas.190206797] [PMID: 11016948]
[34]
Balosso S, Ravizza T, Perego C, et al. Tumor necrosis factor-α inhibits seizures in mice via p75 receptors. Ann Neurol 2005; 57(6): 804-12.
[http://dx.doi.org/10.1002/ana.20480] [PMID: 15852477]
[35]
Ravizza T, Lucas SM, Balosso S, et al. Inactivation of caspase-1 in rodent brain: A novel anticonvulsive strategy. Epilepsia 2006; 47(7): 1160-8.
[http://dx.doi.org/10.1111/j.1528-1167.2006.00590.x] [PMID: 16886979]
[36]
Samland H, Huitron-Resendiz S, Masliah E, Criado J, Henriksen SJ, Campbell IL. Profound increase in sensitivity to glutamatergic- but not cholinergic agonist-induced seizures in transgenic mice with astrocyte production of IL-6. J Neurosci Res 2003; 73(2): 176-87.
[http://dx.doi.org/10.1002/jnr.10635] [PMID: 12836160]
[37]
Akassoglou K, Probert L, Kontogeorgos G, Kollias G. Astrocyte-specific but not neuron-specific transmembrane TNF triggers inflammation and degeneration in the central nervous system of transgenic mice. J Immunol 1997; 158(1): 438-45.
[PMID: 8977220]
[38]
Kelley KA, Ho L, Winger D, et al. Potentiation of excitotoxicity in transgenic mice overexpressing neuronal cyclooxygenase-2. Am J Pathol 1999; 155(3): 995-1004.
[http://dx.doi.org/10.1016/S0002-9440(10)65199-1] [PMID: 10487857]
[39]
De Sarro G, Russo E, Ferreri G, et al. Seizure susceptibility to various convulsant stimuli of knockout interleukin-6 mice. Pharmacol Biochem Behav 2004; 77(4): 761-6.
[http://dx.doi.org/10.1016/j.pbb.2004.01.012] [PMID: 15099921]
[40]
Stojkovska I, Wagner BM, Morrison BE. Parkinson’s disease and enhanced inflammatory response. Exp Biol Med (Maywood) 2015; 240(11): 1387-95.
[http://dx.doi.org/10.1177/1535370215576313] [PMID: 25769314]
[41]
Goldman SM, Tanner CM, Oakes D, Bhudhikanok GS, Gupta A, Langston JW. Head injury and Parkinson’s disease risk in twins. Ann Neurol 2006; 60(1): 65-72.
[http://dx.doi.org/10.1002/ana.20882] [PMID: 16718702]
[42]
Poltorak A, He X, Smirnova I, et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: Mutations in Tlr4 gene. Science 1998; 282(5396): 2085-8.
[http://dx.doi.org/10.1126/science.282.5396.2085] [PMID: 9851930]
[43]
Lu YC, Yeh WC, Ohashi PS. LPS/TLR4 signal transduction pathway. Cytokine 2008; 42(2): 145-51.
[http://dx.doi.org/10.1016/j.cyto.2008.01.006] [PMID: 18304834]
[44]
Castaño A, Herrera AJ, Cano J, Machado A. Lipopolysaccharide intranigral injection induces inflammatory reaction and damage in nigrostriatal dopaminergic system. J Neurochem 1998; 70(4): 1584-92.
[http://dx.doi.org/10.1046/j.1471-4159.1998.70041584.x] [PMID: 9580157]
[45]
Herrera AJ, Castaño A, Venero JL, Cano J, Machado A. The single intranigral injection of LPS as a new model for studying the selective effects of inflammatory reactions on dopaminergic system. Neurobiol Dis 2000; 7(4): 429-47.
[http://dx.doi.org/10.1006/nbdi.2000.0289] [PMID: 10964613]
[46]
Lu X, Bing G, Hagg T. Naloxone prevents microglia-induced degeneration of dopaminergic substantia nigra neurons in adult rats. Neuroscience 2000; 97(2): 285-91.
[http://dx.doi.org/10.1016/S0306-4522(00)00033-6] [PMID: 10799760]
[47]
Hernández-Romero MC, Argüelles S, Villarán RF, et al. Simvastatin prevents the inflammatory process and the dopaminergic degeneration induced by the intranigral injection of lipopolysaccharide. J Neurochem 2008; 105(2): 445-59.
[http://dx.doi.org/10.1111/j.1471-4159.2007.05148.x] [PMID: 18047562]
[48]
Mao LY, Ding J, Peng WF, et al. Interictal interleukin-17A levels are elevated and correlate with seizure severity of epilepsy patients. Epilepsia 2013; 54(9): e142-5.
[http://dx.doi.org/10.1111/epi.12337] [PMID: 23944193]
[49]
Bergantin LB. Common issues among asthma, epilepsy, and schizophrenia: From inflammation to Ca2+/cAMP signalling. Antiinflamm Antiallergy Agents Med Chem 2020. [Epub ahead of print]
[http://dx.doi.org/10.2174/1871523019999201110192029] [PMID: 33176668]
[50]
Caricati-Neto A, García AG, Bergantin LB. Pharmacological implications of the Ca(2+)/cAMP signaling interaction: From risk for antihypertensive therapy to potential beneficial for neurological and psychiatric disorders. Pharmacol Res Perspect 2015; 3(5): e00181.
[http://dx.doi.org/10.1002/prp2.181] [PMID: 26516591]
[51]
Olivier M. Modulation of host cell intracellular Ca2+. Parasitol Today 1996; 12(4): 145-50.
[http://dx.doi.org/10.1016/0169-4758(96)10006-5] [PMID: 15275223]
[52]
Nugent KM, Shanley JD. Verapamil inhibits influenza A virus replication. Arch Virol 1984; 81(1-2): 163-70.
[http://dx.doi.org/10.1007/BF01309305] [PMID: 6743023]
[53]
Dionicio CL, Peña F, Constantino-Jonapa LA, et al. Dengue virus induced changes in Ca2+ homeostasis in human hepatic cells that favor the viral replicative cycle. Virus Res 2018; 245: 17-28.
[http://dx.doi.org/10.1016/j.virusres.2017.11.029] [PMID: 29269104]
[54]
Scherbik SV, Brinton MA. Virus-induced Ca2+ influx extends survival of west nile virus-infected cells. J Virol 2010; 84(17): 8721-31.
[http://dx.doi.org/10.1128/JVI.00144-10] [PMID: 20538858]
[55]
Johansen LM, DeWald LE, Shoemaker CJ, et al. A screen of approved drugs and molecular probes identifies therapeutics with anti-Ebola virus activity. Sci Transl Med 2015; 7(290): 290ra89.
[http://dx.doi.org/10.1126/scitranslmed.aaa5597] [PMID: 26041706]
[56]
Ritz B, Rhodes SL, Qian L, Schernhammer E, Olsen JH, Friis S. L-type calcium channel blockers and Parkinson disease in Denmark. Ann Neurol 2010; 67(5): 600-6.
[PMID: 20437557]
[57]
Bergantin LB. Debating the “bidirectional link” between diabetes and depression through the Ca2+/cAMP signalling: Off-label effects of Ca2+ channel blockers. Pharmacol Res 2019; 141: 298-302.
[http://dx.doi.org/10.1016/j.phrs.2019.01.008] [PMID: 30639385]
[58]
Bergantin LB. Depression rises the risk of hypertension incidence: Discussing the link through the Ca2+/cAMP signalling. Curr Hypertens Rev 2020; 16(1): 73-8.
[http://dx.doi.org/10.2174/1573402115666190116095223] [PMID: 30648516]
[59]
Bergantin LB. A hypothesis for the relationship between depression and cancer: Role of Ca2+/cAMP signalling. Anticancer Agents Med Chem 2020; 20(7): 777-82.
[http://dx.doi.org/10.2174/1871520620666200220113817] [PMID: 32077833]
[60]
Bergantin LB. The clinical link between depression and obesity: Role of Ca2+/cAMP signalling. Psychiatry Res 2020; 291: 113167.
[http://dx.doi.org/10.1016/j.psychres.2020.113167] [PMID: 32562933]
[61]
Bergantin LB. The interactions between Alzheimer´s disease and major depression: Role of Ca2+ channel blockers and Ca2+/cAMP signalling. Curr Drug Res Rev 2020.
[http://dx.doi.org/10.2174/2589977512666200217093356] [PMID: 32065096]
[62]
Ferrendelli JA, Blank AC, Gross RA. Relationships between seizure activity and cyclic nucleotide levels in brain. Brain Res 1980; 200(1): 93-103.
[http://dx.doi.org/10.1016/0006-8993(80)91097-5] [PMID: 6251946]
[63]
Raker VK, Becker C, Steinbrink K. The cAMP pathway as therapeutic target in autoimmune and inflammatory diseases. Front Immunol 2016; 7: 123.
[http://dx.doi.org/10.3389/fimmu.2016.00123] [PMID: 27065076]
[64]
Moore AR, Willoughby DA. The role of cAMP regulation in controlling inflammation. Clin Exp Immunol 1995; 101(3): 387-9.
[http://dx.doi.org/10.1111/j.1365-2249.1995.tb03123.x] [PMID: 7664483]
[65]
Erdogan S, Aslantas O, Celik S, Atik E. The effects of increased cAMP content on inflammation, oxidative stress and PDE4 transcripts during Brucella melitensis infection. Res Vet Sci 2008; 84(1): 18-25.
[http://dx.doi.org/10.1016/j.rvsc.2007.02.003] [PMID: 17397885]
[66]
Tavares LP, Negreiros-Lima GL, Lima KM, et al. Blame the signaling: Role of cAMP for the resolution of inflammation. Pharmacol Res 2020; 159: 105030.
[http://dx.doi.org/10.1016/j.phrs.2020.105030] [PMID: 32562817]
[67]
Catoni C, Calì T, Brini M. Calcium, dopamine and neuronal calcium sensor 1: Their contribution to Parkinson’s disease. Front Mol Neurosci 2019; 12: 55.
[http://dx.doi.org/10.3389/fnmol.2019.00055] [PMID: 30967759]
[68]
Pchitskaya E, Popugaeva E, Bezprozvanny I. Calcium signaling and molecular mechanisms underlying neurodegenerative diseases. Cell Calcium 2018; 70: 87-94.
[http://dx.doi.org/10.1016/j.ceca.2017.06.008] [PMID: 28728834]
[69]
Müller M, Ahumada-Castro U, Sanhueza M, Gonzalez-Billault C, Court FA, Cárdenas C. Mitochondria and calcium regulation as basis of neurodegeneration associated with aging. Front Neurosci 2018; 12: 470.
[http://dx.doi.org/10.3389/fnins.2018.00470] [PMID: 30057523]
[70]
Liss B, Striessnig J. The potential of l-type calcium channels as a drug target for neuroprotective therapy in Parkinson’s disease. Annu Rev Pharmacol Toxicol 2019; 59: 263-89.
[http://dx.doi.org/10.1146/annurev-pharmtox-010818-021214] [PMID: 30625283]
[71]
Di Filippo L, Formenti AM, Rovere-Querini P, et al. Hypocalcemia is highly prevalent and predicts hospitalization in patients with COVID-19. Endocrine 2020; 68(3): 475-8.
[http://dx.doi.org/10.1007/s12020-020-02383-5] [PMID: 32533508]
[72]
Liu J, Han P, Wu J, Gong J, Tian D. Prevalence and predictive value of hypocalcemia in severe COVID-19 patients. J Infect Public Health 2020; 13(9): 1224-8.
[http://dx.doi.org/10.1016/j.jiph.2020.05.029] [PMID: 32622796]
[73]
Wu Y, Hou B, Liu J, Chen Y, Zhong P. Risk factors associated with long-term hospitalization in patients with COVID-19: A single-centered, retrospective study. Front Med (Lausanne) 2020; 7: 315.
[http://dx.doi.org/10.3389/fmed.2020.00315] [PMID: 32582749]
[74]
di Filippo L, Formenti AM, Giustina A. Hypocalcemia: The quest for the cause of a major biochemical feature of COVID-19. Endocrine 2020; 70(3): 463-4.
[http://dx.doi.org/10.1007/s12020-020-02525-9] [PMID: 33094473]
[75]
Williams GC, Nesse RM. The dawn of Darwinian medicine. Q Rev Biol 1991; 66(1): 1-22.
[http://dx.doi.org/10.1086/417048] [PMID: 2052670]
[76]
Aberegg SK. Ionized calcium in the ICU: Should it be measured and corrected? Chest 2016; 149(3): 846-55.
[http://dx.doi.org/10.1016/j.chest.2015.12.001] [PMID: 26836894]
[77]
LeGrand EK, Alcock J. Turning up the heat: Immune brinksmanship in the acute-phase response. Q Rev Biol 2012; 87(1): 3-18.
[http://dx.doi.org/10.1086/663946] [PMID: 22518930]
[78]
Collage RD, Howell GM, Zhang X, et al. Calcium supplementation during sepsis exacerbates organ failure and mortality via calcium/calmodulin-dependent protein kinase kinase signaling. Crit Care Med 2013; 41(11): e352-60.
[http://dx.doi.org/10.1097/CCM.0b013e31828cf436] [PMID: 23887235]
[79]
Dotson B, Larabell P, Patel JU, et al. Calcium administration is associated with adverse outcomes in critically ill patients receiving parenteral nutrition: Results from a natural experiment created by a calcium gluconate shortage. Pharmacotherapy 2016; 36(11): 1185-90.
[http://dx.doi.org/10.1002/phar.1849] [PMID: 27732742]
[80]
He W, An Y, Huang L, et al. Calcium supplementation prolongs the time of hospitalization and has a double effect on mortality in septic patients: A retrospective study from MIMIC-III. Research Square 2020; 2020: 1-26.
[http://dx.doi.org/10.21203/rs.3.rs-16486/v1]
[81]
Malcolm DS, Zaloga GP, Holaday JW. Calcium administration increases the mortality of endotoxic shock in rats. Crit Care Med 1989; 17(9): 900-3.
[http://dx.doi.org/10.1097/00003246-198909000-00012] [PMID: 2504540]
[82]
Zaloga GP, Sager A, Black KW, Prielipp R. Low dose calcium administration increases mortality during septic peritonitis in rats. Circ Shock 1992; 37(3): 226-9.
[PMID: 1423913]
[83]
Klein P, Friedman A, Hameed MQ, et al. Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy? Epilepsia 2020; 61(3): 359-86.
[http://dx.doi.org/10.1111/epi.16450] [PMID: 32196665]
[84]
Hung AY, Schwarzschild MA. Approaches to disease modification for Parkinson’s disease: Clinical trials and lessons learned. Neurotherapeutics 2020; 17(4): 1393-405.
[http://dx.doi.org/10.1007/s13311-020-00964-w] [PMID: 33205384]
[85]
Swart T, Hurley MJ. Calcium channel antagonists as disease-modifying therapy for Parkinson’s disease: Therapeutic rationale and current status. CNS Drugs 2016; 30(12): 1127-35.
[http://dx.doi.org/10.1007/s40263-016-0393-9] [PMID: 27826740]
[86]
Zamponi GW. Targeting voltage-gated calcium channels in neurological and psychiatric diseases. Nat Rev Drug Discov 2016; 15(1): 19-34.
[http://dx.doi.org/10.1038/nrd.2015.5] [PMID: 26542451]
[87]
Bhat A, Ray B, Mahalakshmi AM, et al. Phosphodiesterase-4 enzyme as a therapeutic target in neurological disorders. Pharmacol Res 2020; 160: 105078.
[http://dx.doi.org/10.1016/j.phrs.2020.105078] [PMID: 32673703]

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