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Current Drug Research Reviews

Editor-in-Chief

ISSN (Print): 2589-9775
ISSN (Online): 2589-9783

Mini-Review Article

Potential of Antibiotics for the Treatment and Management of Parkinson's Disease: An Overview

Author(s): Narayan Yadav, Ajit Kumar Thakur*, Nikhila Shekhar and Ayushi

Volume 13, Issue 3, 2021

Published on: 14 March, 2021

Page: [166 - 171] Pages: 6

DOI: 10.2174/2589977513666210315095133

Price: $65

Abstract

Evidence has emerged over the last 2 decades to ascertain the proof of concepts viz. mitochondrial dysfunction, inflammation-derived oxidative damage and cytokine-induced toxicity that play a significant role in Parkinson's disease (PD). The available pharmacotherapies for PD are mainly symptomatic and typically indicate L-DOPA to restrain dopamine deficiency and its consequences. In the 21st century, the role of antibiotics has emerged at the forefront of medicines in health and human illness. There are several experimental and pre-clinical evidences that support the potential use of antibiotics as a neuroprotective agent. The astonishing effects of antibiotics and their neuroprotective properties against neurodegeneration and neuro-inflammation would be phenomenal for the development of effective therapy against PD. Antibiotics are also testified as useful in not only preventing the formation of alpha-synuclein but also acting on mitochondrial dysfunction and neuro-inflammation. Thus, the possible therapy with antibiotics in PD would impact both pathways leading to neuronal cell death in substantia nigra and pars compacta in the midbrain. Moreover, the antibiotic-based pharmacotherapy will open a scientific research avenue to add more to the evidence-based and rational use of antibiotics for the treatment and management of PD and other neurodegenerative disorders.

Keywords: Antibiotic, neuro-inflammation, neurodegeneration, oxidative damage, parkinson's disease, neuroprotection.

Graphical Abstract
[1]
Braak H, Del Tredici K, Rüb U, de Vos RA, Jansen Steur EN, Braak E. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiol Aging 2003; 24(2): 197-211.
[http://dx.doi.org/10.1016/S0197-4580(02)00065-9] [PMID: 12498954]
[2]
Kakkar AK, Dahiya N. Management of Parkinson׳s disease: Current and future pharmacotherapy. Eur J Pharmacol 2015; 750: 74-81.
[http://dx.doi.org/10.1016/j.ejphar.2015.01.030] [PMID: 25637088]
[3]
Dorszewska J, Prendecki M, Lianeri M, Kozubski W. Molecular effects of l-dopa therapy in Parkinson’s disease. Curr Genomics 2014; 15(1): 11-7.
[http://dx.doi.org/10.2174/1389202914666131210213042] [PMID: 24653659]
[4]
Vanle B, Olcott W, Jimenez J, Bashmi L, Danovitch I, IsHak WW. NMDA antagonists for treating the non-motor symptoms in Parkinson’s disease. Transl Psychiatry 2018; 8(1): 117.
[http://dx.doi.org/10.1038/s41398-018-0162-2] [PMID: 29907742]
[5]
Marvel CL, Paradiso S. Cognitive and neurological impairment in mood disorders. Psychiatr Clin North Am 2004; 27(1): 19-36.
[http://dx.doi.org/10.1016/S0193-953X(03)00106-0] [PMID: 15062628]
[6]
Morphy R, Rankovic Z. Designing multiple ligands - medicinal chemistry strategies and challenges. Curr Pharm Des 2009; 15(6): 587-600.
[http://dx.doi.org/10.2174/138161209787315594] [PMID: 19199984]
[7]
Van der Schyf CJ, Youdim MB. Multifunctional drugs as neurotherapeutics. Neurotherapeut 2009; 6(1): 1-3.
[http://dx.doi.org/10.1016/j.nurt.2008.11.001] [PMID: 19110194]
[8]
Wang G, Qi C, Fan GH, Zhou HY, Chen SD. PACAP protects neuronal differentiated PC12 cells against the neurotoxicity induced by a mitochondrial complex I inhibitor, rotenone. FEBS Lett 2005; 579(18): 4005-11.
[http://dx.doi.org/10.1016/j.febslet.2005.06.013] [PMID: 16004991]
[9]
Li J, Zhu M, Rajamani S, Uversky VN, Fink AL. Rifampicin inhibits alpha-synuclein fibrillation and disaggregates fibrils. Chem Biol 2004; 11(11): 1513-21.
[http://dx.doi.org/10.1016/j.chembiol.2004.08.025] [PMID: 15556002]
[10]
Beretta L, Gingras AC, Svitkin YV, Hall MN, Sonenberg N. Rapamycin blocks the phosphorylation of 4E-BP1 and inhibits CAP-dependent initiation of translation. EMBO J 1996; 15(3): 658-64.
[http://dx.doi.org/10.1002/j.1460-2075.1996.tb00398.x] [PMID: 8599949]
[11]
Pang SY, Ho PW, Liu HF, et al. The interplay of aging, genetics and environmental factors in the pathogenesis of Parkinson’s disease. Transl Neurodegener 2019; 8: 23.
[http://dx.doi.org/10.1186/s40035-019-0165-9] [PMID: 31428316]
[12]
Duvoisin RC. Recent advances in the genetics of Parkinson’s disease. Adv Neurol 1996; 69: 33-40.
[PMID: 8615148]
[13]
Pollanen MS, Dickson DW, Bergeron C. Pathology and biology of the Lewy body. J Neuropathol Exp Neurol 1993; 52(3): 183-91.
[http://dx.doi.org/10.1097/00005072-199305000-00001] [PMID: 7684074]
[14]
Patt S, Gertz HJ, Gerhard L, Cervós-Navarro J. Pathological changes in dendrites of substantia nigra neurons in Parkinson’s disease: a Golgi study. Histol Histopathol 1991; 6(3): 373-80.
[PMID: 1725760]
[15]
Hartmann A. Postmortem studies in Parkinson’s disease. Dialogues Clin Neurosci 2004; 6(3): 281-93.
[http://dx.doi.org/10.31887/DCNS.2004.6.3/ahartmann] [PMID: 22033507]
[16]
Damier P, Hirsch EC, Agid Y, Graybiel AM. The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurons in Parkinson’s disease. Brain 1999; 122(Pt 8): 1437-48.
[http://dx.doi.org/10.1093/brain/122.8.1437] [PMID: 10430830]
[17]
Zigmond MJ. Chemical transmission in the brain: homeostatic regulation and its functional implications. Prog Brain Res 1994; 100: 115-22.
[http://dx.doi.org/10.1016/S0079-6123(08)60776-1] [PMID: 7938509]
[18]
Barber M, Stewart D, Grosset D, MacPhee G. Patient and carer perception of the management of Parkinson’s disease after surgery. Age Ageing 2001; 30(2): 171-2.
[http://dx.doi.org/10.1093/ageing/30.2.171-a] [PMID: 11395349]
[19]
Chavez-Valdez R. Repurposing azithromycin for neuroprotection in neonates. Pediatr Res 2019; 86(4): 423-4.
[http://dx.doi.org/10.1038/s41390-019-0443-3] [PMID: 31129682]
[20]
Pradhan S, Andreasson K. Commentary: progressive inflammation as a contributing factor to early development of Parkinson’s disease. Exp Neurol 2013; 241: 148-55.
[http://dx.doi.org/10.1016/j.expneurol.2012.12.008] [PMID: 23261765]
[21]
Schinder AF, Olson EC, Spitzer NC, Montal M. Mitochondrial dysfunction is a primary event in glutamate neurotoxicity. J Neurosci 1996; 16(19): 6125-33.
[http://dx.doi.org/10.1523/JNEUROSCI.16-19-06125.1996] [PMID: 8815895]
[22]
Zhang B, Bailey WM, Kopper TJ, Orr MB, Feola DJ, Gensel JC. Azithromycin drives alternative macrophage activation and improves recovery and tissue sparing in contusion spinal cord injury. J Neuroinflammation 2015; 12: 218.
[http://dx.doi.org/10.1186/s12974-015-0440-3] [PMID: 26597676]
[23]
Acocella G. Clinical pharmacokinetics of rifampicin. Clin Pharmacokinet 1978; 3(2): 108-27.
[http://dx.doi.org/10.2165/00003088-197803020-00002] [PMID: 346286]
[24]
Bi W, Zhu L, Jing X, Liang Y, Tao E. Rifampicin and Parkinson’s disease. Neurol Sci 2013; 34(2): 137-41.
[http://dx.doi.org/10.1007/s10072-012-1156-0] [PMID: 22821065]
[25]
Ryan ME, Greenwald RA, Golub LM. Potential of tetracyclines to modify cartilage breakdown in osteoarthritis. Curr Opin Rheumatol 1996; 8(3): 238-47.
[http://dx.doi.org/10.1097/00002281-199605000-00013] [PMID: 8796985]
[26]
Golub LM, Evans RT, McNamara TF, Lee HM, Ramamurthy NS. A non-antimicrobial tetracycline inhibits gingival matrix metalloproteinases and bone loss in Porphyromonas gingivalis-induced periodontitis in rats. Ann N Y Acad Sci 1994; 732: 96-111.
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb24728.x] [PMID: 7978855]
[27]
Thomas M, Le WD. Minocycline: Neuroprotective mechanisms in Parkinson’s disease. Curr Pharm Des 2004; 10(6): 679-86.
[http://dx.doi.org/10.2174/1381612043453162] [PMID: 14965330]
[28]
Dauer W, Przedborski S. Parkinson’s disease: mechanisms and models. Neuron 2003; 39(6): 889-909.
[http://dx.doi.org/10.1016/S0896-6273(03)00568-3] [PMID: 12971891]
[29]
Yrjänheikki J, Tikka T, Keinänen R, Goldsteins G, Chan PH, Koistinaho J. A tetracycline derivative, minocycline, reduces inflammation and protects against focal cerebral ischemia with a wide therapeutic window. Proc Natl Acad Sci USA 1999; 96(23): 13496-500.
[http://dx.doi.org/10.1073/pnas.96.23.13496] [PMID: 10557349]
[30]
Lin S, Zhang Y, Dodel R, Farlow MR, Paul SM, Du Y. Minocycline blocks nitric oxide-induced neurotoxicity by inhibition p38 MAP kinase in rat cerebellar granule neurons. Neurosci Lett 2001; 315(1-2): 61-4.
[http://dx.doi.org/10.1016/S0304-3940(01)02324-2] [PMID: 11711215]
[31]
Lassus P, Opitz-Araya X, Lazebnik Y. Requirement for caspase-2 in stress-induced apoptosis before mitochondrial permeabilization. Science 2002; 297(5585): 1352-4.
[http://dx.doi.org/10.1126/science.1074721] [PMID: 12193789]
[32]
Tikka T, Usenius T, Tenhunen M, Keinänen R, Koistinaho J. Tetracycline derivatives and ceftriaxone, a cephalosporin antibiotic, protect neurons against apoptosis induced by ionizing radiation. J Neurochem 2001; 78(6): 1409-14.
[http://dx.doi.org/10.1046/j.1471-4159.2001.00543.x] [PMID: 11579149]
[33]
Zhu S, Stavrovskaya IG, Drozda M, et al. Minocycline inhibits cytochrome c release and delays progression of amyotrophic lateral sclerosis in mice. Nature 2002; 417(6884): 74-8.
[http://dx.doi.org/10.1038/417074a] [PMID: 11986668]
[34]
Du Y, Ma Z, Lin S, et al. Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson’s disease. Proc Natl Acad Sci USA 2001; 98(25): 14669-74.
[http://dx.doi.org/10.1073/pnas.251341998] [PMID: 11724929]
[35]
Cankaya S, Cankaya B, Kilic U, Kilic E, Yulug B. The therapeutic role of minocycline in Parkinson’s disease. Drugs Context 2019; 8: 212553.
[http://dx.doi.org/10.7573/dic.212553] [PMID: 30873213]
[36]
Gordon RA, Mays R, Sambrano B, Mayo T, Lapolla W. Antibiotics used in nonbacterial dermatologic conditions. Dermatol Ther (Heidelb) 2012; 25(1): 38-54.
[http://dx.doi.org/10.1111/j.1529-8019.2012.01496.x] [PMID: 22591498]
[37]
Moon A, Gil S, Gill SE, Chen P, Matute-Bello G. Doxycycline impairs neutrophil migration to the airspaces of the lung in mice exposed to intratracheal lipopolysaccharide. J Inflamm (Lond) 2012; 9(1): 31.
[http://dx.doi.org/10.1186/1476-9255-9-31] [PMID: 22943365]
[38]
Wei J, Pan X, Pei Z, et al. The beta-lactam antibiotic, ceftriaxone, provides neuroprotective potential via anti-excitotoxicity and anti-inflammation response in a rat model of traumatic brain injury. J Trauma Acute Care Surg 2012; 73(3): 654-60.
[http://dx.doi.org/10.1097/TA.0b013e31825133c0] [PMID: 22710775]
[39]
Yulug B, Hanoglu L, Ozansoy M, et al. Therapeutic role of rifampicin in Alzheimer’s disease. Psychiatry Clin Neurosci 2018; 72(3): 152-9.
[http://dx.doi.org/10.1111/pcn.12637] [PMID: 29315976]
[40]
Gensel JC, Kopper TJ, Zhang B, Orr MB, Bailey WM. Predictive screening of M1 and M2 macrophages reveals the immunomodulatory effectiveness of post spinal cord injury azithromycin treatment. Sci Rep 2017; 7: 40144.
[http://dx.doi.org/10.1038/srep40144] [PMID: 28057928]
[41]
Amantea D, Certo M, Petrelli F, et al. Azithromycin protects mice against ischemic stroke injury by promoting macrophage transition towards M2 phenotype. Exp Neurol 2016; 275(Pt 1): 116-25.
[http://dx.doi.org/10.1016/j.expneurol.2015.10.012] [PMID: 26518285]
[42]
Hodge S, Tran HB, Hamon R, et al. Nonantibiotic macrolides restore airway macrophage phagocytic function with potential anti-inflammatory effects in chronic lung diseases. Am J Physiol Lung Cell Mol Physiol 2017; 312(5): L678-87.
[http://dx.doi.org/10.1152/ajplung.00518.2016] [PMID: 28258107]
[43]
Zhang B, Kopper TJ, Liu X, Cui Z, Van Lanen SG, Gensel JC. Macrolide derivatives reduce proinflammatory macrophage activation and macrophage-mediated neurotoxicity. CNS Neurosci Ther 2019; 25(5): 591-600.
[http://dx.doi.org/10.1111/cns.13092] [PMID: 30677254]
[44]
Bosnar M, Kragol G, Koštrun S, et al. N′-substituted-2′-O,3′-N-carbonimidoyl bridged macrolides: novel anti-inflammatory macrolides without antimicrobial activity. J Med Chem 2012; 55(13): 6111-23.
[http://dx.doi.org/10.1021/jm300356u] [PMID: 22697905]
[45]
Sugawara A, Sueki A, Hirose T, et al. Novel 12-membered non-antibiotic macrolides from erythromycin A; EM900 series as novel leads for anti-inflammatory and/or immunomodulatory agents. Bioorg Med Chem Lett 2011; 21(11): 3373-6.
[http://dx.doi.org/10.1016/j.bmcl.2011.04.004] [PMID: 21524580]
[46]
Mencarelli A, Distrutti E, Renga B, et al. Development of non-antibiotic macrolide that corrects inflammation-driven immune dysfunction in models of inflammatory bowel diseases and arthritis. Eur J Pharmacol 2011; 665(1-3): 29-39.
[http://dx.doi.org/10.1016/j.ejphar.2011.04.036] [PMID: 21554873]
[47]
Rodriguez CC, Sanchez BE, Molares VA. Clinical application of development of nonantibiotic macrolides that correct inflammation-driven immune dysfunction in inflammatory skin diseases. Mediators Inflamm 2012; 2012: 563709.
[http://dx.doi.org/10.1155/2012/563709] [PMID: 23258954]
[48]
Amantea D, Petrelli F, Greco R, et al. Azithromycin affords neuroprotection in rat undergone transient focal cerebral ischemia. Front Neurosci 2019; 13: 1256.
[http://dx.doi.org/10.3389/fnins.2019.01256] [PMID: 31849581]
[49]
Balloy V, Deveaux A, Lebeaux D, et al. Azithromycin analogue CSY0073 attenuates lung inflammation induced by LPS challenge. Br J Pharmacol 2014; 171(7): 1783-94.
[http://dx.doi.org/10.1111/bph.12574] [PMID: 24417187]

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