Neuroprotective antibiotics in Alzheimer´s disease.

María Rodríguez-Pérez, Cristina Pintado, Oscar Gómez, Emma Burgos-Ramos

Abstract


Alzheimer´s disease (AD) is an irreversible neurodegenerative disorder and one of the main aging-dependent maladies of the 21st century. Currently, around of 46 million people suffer from AD worldwide, and these data will be duplicate in 20 years. Due to the progressive aging of the population and the prediction of an increase in the incidence of this disease, AD constitutes a serious familiar and socio-sanitary problem. Therefore, it is essential to find therapeutic strategies which are addressed to prevent, delay the onset, slow the progression and /or improve the symptoms of AD. Nowadays, the research lines focus on finding and identifying new drugs for reaching these improvements. In this article we have focused on review thoroughly the neuroprotective role, in AD of the antibiotics rifampicin, rapamycin and minocycline, because they reach quickly the brain and are very cheap. Likewise, we have found evidences both “in vitro” and “in vivo” studies, even some clinical trials about it, but minority. In a general view, all the antibiotics reviewed exert neuroprotection, because they act as an anti-inflammatory and anti-amyloidogenic agents. 


Keywords


Alzheimer’s disease; antibiotics; neuroprotection

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References


Walsh, D.M., et al., Deciphering the molecular basis of memory failure in Alzheimer's disease. Neuron, 2004. 44(1): p.181-193.

Sambamurti, K., et al., Advances in the cellular and molecular biology of the beta-amyloid protein in Alzheimer's disease. Neuromol Med, 2002. 1(1): p. 1-31.

Pintado, C., et al., Neuroinflammation alters cellular proteostasis by producing endoplasmic reticulum stress, autophagy activation and disrupting ERAD activation. Sci Rep. 2017. 7(1): p. 8100.

Freeman, L.C., et al., The pathogenic role of the inflammasome in neurodegenerative diseases. J Neurochem, 2016. 136(1): p. 29-38.

Mandrekar-Colucci, S., et al., Microglia and inflammation in Alzheimer’s disease. CNS & Neurol Disord – Drug Targets, 2010. 9(2): p. 156-167.

Crespo, C., et al., Hydroxytyrosol restores proper insulin signaling in an astrocytic model of Alzheimer's disease. Biofactors, 2017. 43(4): p. 540-548.

Sarubbo, F., et al., Effects of Resveratrol and other Polyphenols on the most common Brain Age-Related Diseases. Curr Med Chem, 2017. doi:10.2174/0929867324666170724102743.

Zhang, Y.P., et al., DHA, EPA and their combination at various ratios differently modulated Aβ25-35-induced neurotoxicity in SH-SY5Y cells. Prostaglandins Leukot Essent Fatty Acids. 2017. pii: S0952-3278(17)30026-1. doi:10.1016/j.plefa.2017.07.003.

Ortiz-López, L., et al., Green tea compound epigallo-catechin-3-gallate (EGCG) increases neuronal survival in adult hippocampal neurogenesis in vivo and in vitro. Neuroscience. 2016. 322: p. 208-220.

Wang, Y., Effects of caffeic acid on learning deficits in a model of Alzheimer's disease. Int J Mol Med, 2016. 38(3): p. 869-875.

Shobo, A., et al., Visualization of Time-Dependent Distribution of Rifampicin in Rat Brain Using MALDI MSI and Quantitative LCMS/MS. Assay Drug Dev Technol, 2015. 13(5): p. 277-284.

Aronson, A.L., Pharmacotherapeutics of newer tetracyclines. J Am Vet Med Assoc, 1980. 176(10 Spec No): p. 1061-1080.

Tomiyama, T. et al., Rifampicin prevents the aggregation and neurotoxicity of amyloid β protein in vitro. Biochem and Biophys Res Commun, 1994. 204(1): p. 76-83.

Tomiyama, T., et al., Inhibition of amyloid beta protein aggregation and neurotoxicity by rifampicin. Its possible function as a hydroxyl radical scavenger. J Biol Chem, 1996. 271(12): p. 6839–6844.

Tomiyama, T., et al., 1997). Rifampicin inhibits the toxicity of pre-aggregated amyloid ppetides by binding to peptide fibrils and preventing amyloid-cell interaction. Biochem J, 1997. 322( Pt 3): p. 859–865.

Balali-Mood, K., et al., Neutron diffraction reveals sequence-specific membrane insertion of pre-fibrillar islet amyloid polypeptide and inhibition by rifampicin. FEBS Letters, 2005. 579(5): p. 1143–1148.

Findeis, M.A., Approaches to discovery and characterization of inhibitors of amyloid beta-peptide polymerization. ‎Biochim Biophys Acta, 2000. 1502(1): p. 76-84.

Qosa, H., et al., Enhanced brain amyloid-β clearance by rifampycin and caffeine as a possible protective mechanism against Alzheimer´s disease. ‎J. Alzheimers Dis:JAD, 2012. 31(1): p. 151-165.

Abuznait, A. H., et al., Up-regulation of P-glycoprotein reduces intracellular accumulation of beta amyloid: investigation of P-glycoprotein as a novel therapeutic target for Alzheimer´s disease. J Pharm Pharmacol, 2011. 63(8): p. 1111-1118.

Bi, W., et al., Rifampicin inhibits microglial inflammation and improves neuron survival against inflammation. Brain Research, 2011. 1395: p. 12-20.

Yulug, B., et al., RIFAMPICIN:An antibiotic with brain protective function. Brain Res Bull, 2014. 107: p. 37-42.

Esposito, E., et al., New therapeutic strategy for Parkinson´s and Alzheimer´s disease. Curr Med Chem, 2010. 17(25): p. 2764-2774.

Rifampin, Tuberculosis, 2008. 88(2): p. 151–154.

Umeda, T., et al., Rifampicin is a candidate preventive medicine against amyloid-β and tau oligomers. Brain, 2016. 139(5): p. 1568-1586.

McGeer, P. L., et al., Anti-inflammatory agents as a therapeutic approach to Alzheimer´s disease. Neurology, 1992. 42(2): p. 447-449.

Chui, D. H., et al., Decreased bea-amyloid and increased abnormal Tau deposition in the brain of aged patients with leprosy. Am J Pathol, 1994. 145(4): p. 771-775.

Namba, Y., et al., Neurofibrillary tangles and senile plaques in brain of elderly leprosy patients. Lancet, 1992. 340(8825): p. 978.

Loeb, M. B., et al., A randomized, controlled trial of doxycycline and rifampicin for patients with Alzheimer´s disease. J Am Geriatr Soc, 2004. 52(3): p. 381-387.

Molloy, D., et al., A multicenter, blinded, randomized, factorial controlled trial of doxycycline and rifampin for treatment of Alzheimer´s disease: the DARAD trial. Int J Geriatr Psychiatry, 2013. 28(5): p. 463-470.

Iizuka, T., et al., Preventive effect of rifampicin on Alzheimer disease needs at least 450 mg daily for 1 year: An FDG-PET follow-up study. Dement Geriatr Cogn Disord, 2017. 7(2): p. 204-214.

Vézina, C., et al., A new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle. J Antibiot, 1975. 28: p. 721-726.

Camardo, J., et al., The journes from the laboratory to clinical transplantation. Transplant Proc, 2003. 35: p. 18S-24.

Jia, K., et al. Autophagy is required for dietary restriction-mediated life span extensión in C. elegans. Autofagy, 2007. 3: p. 597-599.

Kapahi, P., et al. Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. Curr. Biol., 2004. 14: p. 885-890.

Harrison, D. E., et al. Rapamycin fed late in life stends lifespan in genetically heterogeneous mice. Nature, 2009. 460: p. 392-395.

Stanfel, M. N., et al. The TOR pathway comes of age. Biochim.Biophys Acta, 2009. 1790: p. 1067-1074.

Hay N., et al. Upstream of mTOR. Genes Dev, 2004. 18: p. 1926-1945.

Caccamo, A., et al., Genetic reduction of mammalian target of rapamycin ameliorates Alzheimer´s disease-like cognitive and pathological déficits by restoring hippocampal gene expression signature. J Neurosci, 2014. 34: p. 7988-7998.

Caccamo, A., et al., Reducing ribosomal protein S6 kinase 1 expression improves spatioal memory and synaptic plasticity in a mouse model of Alzheimer´s disease. J Neurosci, 2015. 285: p.13107-13120.

Caccamo, A., et al., Molecular interplay between mammalian target of rapamycin (mTOR), amyloid-beta, and Tau: effects on cognitive impairments. J Biol Chem, 2010. 285: p. 13107-13120.

Spilman, P., et al., Inhibition of mTOR by rapamycin abolishes cognitive déficits and reduces amyloid-beta levels in a mouse model of Alzheimer´s disease. PLOS One, 2010. 5: e9979.

Zhou, M., et al., mTOR inhibition ameliorates cognitive and affective déficits caused by Disc1 knockdown in adult-born N dentate granule neurons. Neuron, 2013. 77: p. 647-654.

Jung, C. H., et al., ULK-Atg13-FIP200 complexes mediate mTOR signaling to the autophagy machinery. Mol Biol Cell, 2009. 20(7): p. 1992-2003.

Lang U. E., et al., Immunossuppression using the mammalian target of rapamycin (mTOR) inhibitor everolimus: pilot sutudy whows significant cognitive and affective improvement. Transplant Proc, 2009. 41: p. 4285-4288.

Tischmeyer W., et al., Rapamycin-sensitive signalling in long-term cosolidation of auditory cortex-dependent memory. Eur J Neurosci, 2003. 18: p. 942-950.

Schwab, C., et al., Inflammatory aspects of Alzheimer disease and other neurodegenerative disorders. J Alzheimers Dis. 2008. 13: p. 359–369.

Yrjänheikki, J., et al., A tetracycline derivative, minocycline, reduces inflammation and protects against focal cerebral ischemia with a wide therapeutic window. Proc Natl Acad Sci U S A, 1999. 96(23): p. 13496-13500.

Wang, A. L., et al., Minocycline inhibits LPS-induced retinal microglia activation. Neurochem Int, 2005. 47(1-2): p. 152-158.

Kim, SS., et al., Inhibitory action of minocycline on lipopolysaccharide-induced release of nitric oxide and prostaglandin E2 in BV2 microglial cells. Arch Pharm Res, 2004. 27(3):314-318.

Fan, L. W., et al., Minocycline attenuates lipopolysaccharide-induced white matter injury in the neonatal rat brain. Neuroscience, 2005. 133(1): p. 159-168.

Hunter, C. L., et al., Minocycline protects basal forebrain cholinergic neurons from mu p75-saporin immunotoxic lesioning. Eur J Neurosci, 2004. 19: p. 3305–3316.

Garcez, M. L., et al., Minocycline reduces inflammatory parameters in the brain structures and serum and reverses memory impairment caused by the administration of amyloid β (1-42) in mice. Prog Neuropsychopharmacol Biol Psychiatry, 2017. 77: p. 23-31.

Seabrook, T. J., et al., Minocycline affects microglial activation, Aβ-deposition and behavior in APP-tg mice. Glia, 2006. 53: p. 776–782.

Familian, A., et al., Inhibitory effect of minocycline on amyloid beta fibril formation and human microglial activation. Glia, 2006. 53(3): p. 233-240.

Ferretti, M. T., et al., Minocycline corrects early, pre-plaque neuroinflammation and inhibits BACE-1 in a transgenic model of Alzheimer's disease-like amyloid pathology. J Neuroinflammation, 2012. 9: p. 62.

Burgos-Ramos, E., et al., Minocycline prevents Abeta(25-35)-induced reduction of somatostatin and neprilysin content in rat temporal cortex. Life Sci, 2009. 84(7-8): p. 205-210.

Familian, A., et al., Minocycline does not affect amyloid beta phagocytosis by human microglial cells. Neurosci Lett, 2007. 416(1): p. 87-91.

El-Shimy, I. A., et al., Minocycline attenuates Aβ oligomers-induced pro-inflammatory phenotype in primary microglia while enhancing Aβ fibrils phagocytosis. Neurosci Lett, 2015. 609: p. 36-41.

Davies, P., et al., Reduced somatostatin-like immunoreactivity in cerebral cortex from cases of Alzheimer disease and Alzheimer senile dementia. Nature, 1980. 288(5788): p. 279-280.

Nordberg, A., Neuroreceptor changes in Alzheimer disease. Cerebrovasc Brain Metab Rev, 1992. 4(4): p. 303-328.

Burgos-Ramos, E., et al., Minocycline provides protection against beta-amyloid (25-35)-induced alterations of the somatostatin signaling pathway in the rat temporal cortex. Neuroscience, 2008. 154(4): p. 1458-1466.

Zhang, L., et al., Protective effects of minocycline on 3,4 methylenedioxymethamphetamine-induced neurotoxicity in serotonergic and dopaminergic neurons of mouse brain. Eur J Pharmacol, 2006. 544(1-3): p. 1-9.

Du, Y., et al., Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson´s disease. Proc Natl Acad Sci USA, 2001. 98(25): p. 14669-14674.

Chowdhury, R., et al., Dopamine modulates episodic memory persistence in old age. J Neurosci, 2012. 32(41): p. 14193-14204.

Noble, W., et al., Minocycline reduces the development of abnormal tau species in models of Alzheimer´s disease. FASEB J, 2009. 23(3): p. 739-750.

Biscaro, B., et al., Inhibition of microglial activation protects hippocampal neurogenesis and improves cognitive deficits in a transgenic mouse model for Alzheimer´s disease. Neurodegener Dis, 2012. 9(4): p. 187.198.

Parachikova, A., et al., Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylation. J Alzheimers Dis, 2010. 21(2): p. 527-542.

Morse, L. J., et al., FDA-preapproved drugs targeted to the translational regulation and processing of the amyloid precursor protein. J Mol Neurosci, 2004. 24(1): p. 129-136.

Tucker, S., et al., RNA therapeutics directed to the non-coding regions of APP mRNA, in vivo anti-amyloid efficacy of paroxetine, erythromycin, and N-acetyl cysteine. Curr Alzheimer Res, 2006. 3(3): p. 221-227.

Hartsel, S. C., et al., Amphotericin B binds to amyloid fibrils and delays their formation: a therapeutic mechanism? Biochemistry, 2003. 42(20): p. 6228-6233.




DOI: http://dx.doi.org/10.18103/imr.v3i12.599

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