beta-lactam antibiotics as a possible novel therapy for managing epilepsy and autism, a case report and review of literature
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how to cite this article: ghanizadeh a, berk m. beta-lactam antibiotics as a possible novel therapy for managing epilepsy and autism, a case report and review of literature. iran j child neurol. 2015 winter;9(1):99-102. abstract autism is a disorder of unknown etiology. there are few fda approved medications for treating autism. co-occurring autism and epilepsy is common, and glutamate antagonists improve some symptoms of autism. ceftriaxone, a beta-lactam antibiotic, increases the expression of the glutamate transporter 1 which decreases extracellular glutamate levels. it is hypothesized that modulating astrocyte glutamate transporter expression by ceftriaxone or cefixime might improve some symptoms of autism. this case report of a child with autism and epilepsy suggests a decrease in seizures after taking cefixime. references selassie aw, wilson da, martz gu, smith gg, wagner jl, wannamaker bb. epilepsy beyond seizure: a population-based study of comorbidities. epilepsy res 2014;108(2): 305-315. sansa g, carlson c, doyle w, weiner hl, bluvstein, barr w, et al. medically refractory epilepsy in autism. epilepsia 2011; 52(6): 1071-1075. ghanizadeh a. increased glutamate and homocysteine and decreased glutamine levels in autism: a review and strategies for future studies of amino acids in autism. dis markers; 2013;35(5): 281-286. yamada t, kawahara k, kosugi t, tanaka m.nitric oxide produced during sublethal ischemia is crucial for the preconditioning-induced down-regulation of glutamate transporter glt-1 in neuron/astrocyte co-cultures. neurochem res 2006:31(1): 49-56. zeng, lh, ouyang y, gazit v, cirrito jr, jansen la, ess kc, et al. abnormal glutamate homeostasis and impaired synaptic plasticity and learning in a mouse model of tuberous sclerosis complex. neurobiol dis 2007; 28(2): 184-196. zeng lh, bero aw, zhang b, holtzman d. m. , wong m. modulation of astrocyte glutamate transporters decreases seizures in a mouse model of tuberous sclerosis complex. neurobiol dis 2010; 37(3): 764-771. nizzardo m, nardini m, ronchi d, salani s, donadoni c, fortunato f, et al. beta-lactam antibiotic offers neuroprotection in a spinal muscular atrophy model by multiple mechanisms. experimental neurology 2011; 229: 214–225. harada m, taki mm, nose a, kubo h, mori k, nishitani h and t. matsuda. non-invasive evaluation of the gabaergic/glutamatergic system in autistic patients observed by mega-editing proton mr spectroscopy using a clinical 3 tesla instrument. j autism dev disord 2010 apr;41(4):447-54. doi: 10.1007/s10803-010-1065- 0. polleux, f. and j. m. lauder. toward a developmental neurobiology of autism. ment retard dev disabil res rev 2004;10(4): 303-317. maezawa i, jin lw. rett syndrome microglia damage dendrites and synapses by the elevated release of glutamate. j neurosci 2010;30(15): 5346-5356. ghanizadeh a. targeting neurotensin as a potential novel approach for the treatment of autism. j neuroinflammation 2010;7(1): 58. ghanizadeh a. transplantation of gabaergic cell line as a novel hypothesized treatment for autism. epilepsy & behavior 2010;19(4): 664. kim sy, jones ta. the effects of ceftriaxone on skill learning and motor functional outcome after ischemic cortical damage in rats. restor neurol neurosci 2013;31(1):87-97. doi: 10.3233/rnn-2012-120245. ghanizadeh a.could fever and neuroinflammation play a role in the neurobiology of autism? 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منابع مشابه
Beta-Lactam Antibiotics as A Possible Novel Therapy for Managing Epilepsy and Autism, A Case Report and Review of Literature
Autism is a disorder of unknown etiology. There are few FDA approved medications for treating autism. Co-occurring autism and epilepsy is common, and glutamate antagonists improve some symptoms of autism. Ceftriaxone, a beta-lactam antibiotic, increases the expression of the glutamate transporter 1 which decreases extracellular glutamate levels. It is hypothesized that modulating astrocyte glut...
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iranian journal of child neurologyجلد ۹، شماره ۱، صفحات ۹۹-۱۰۲
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