Browsing by Subject "Fluoxetine"

Now showing 1 - 3 of 3
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    Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors
    (Wiley, 2015-08) Hicks, J. Kevin; Bishop, Jeffrey R.; Sangkuhl, Katrin; Müller, Daniel J; Ji, Yuan; Leckband, Susan G.; Leeder, J. Steven; Graham, Rebecca L.; Chiulli, Dana L.; LLerena, Adrián; Skaar, Todd C.; Scott, Stuart A.; Stingl, Julia C.; Klein, Teri E.; Caudle, Kelly E.; Gaedigk, Andrea; Department of Medicine, IU School of Medicine
    Selective serotonin reuptake inhibitors (SSRIs) are primary treatment options for major depressive and anxiety disorders. CYP2D6 and CYP2C19 polymorphisms can influence the metabolism of SSRIs, thereby affecting drug efficacy and safety. We summarize evidence from the published literature supporting these associations and provide dosing recommendations for fluvoxamine, paroxetine, citalopram, escitalopram, and sertraline based on CYP2D6 and/or CYP2C19 genotype (updates at www.pharmgkb.org).
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    Early Chronic Fluoxetine Treatment of Ts65Dn Mice Rescues Synaptic Vesicular Deficits and Prevents Aberrant Proteomic Alterations
    (MDPI, 2024-04-03) Fatemi, S. Hossein; Otte, Elysabeth D.; Folsom, Timothy D.; Eschenlauer, Arthur C.; Roper, Randall J.; Aman, Justin W.; Thuras, Paul D.; Biology, School of Science
    Down syndrome (DS) is the most common form of inherited intellectual disability caused by trisomy of chromosome 21, presenting with intellectual impairment, craniofacial abnormalities, cardiac defects, and gastrointestinal disorders. The Ts65Dn mouse model replicates many abnormalities of DS. We hypothesized that investigation of the cerebral cortex of fluoxetine-treated trisomic mice may provide proteomic signatures that identify therapeutic targets for DS. Subcellular fractionation of synaptosomes from cerebral cortices of age- and brain-area-matched samples from fluoxetine-treated vs. water-treated trisomic and euploid male mice were subjected to HPLC-tandem mass spectrometry. Analysis of the data revealed enrichment of trisomic risk genes that participate in regulation of synaptic vesicular traffic, pre-synaptic and post-synaptic development, and mitochondrial energy pathways during early brain development. Proteomic analysis of trisomic synaptic fractions revealed significant downregulation of proteins involved in synaptic vesicular traffic, including vesicular endocytosis (CLTA, CLTB, CLTC), synaptic assembly and maturation (EXOC1, EXOC3, EXOC8), anterograde axonal transport (EXOC1), neurotransmitter transport to PSD (SACM1L), endosomal-lysosomal acidification (ROGDI, DMXL2), and synaptic signaling (NRXN1, HIP1, ITSN1, YWHAG). Additionally, trisomic proteomes revealed upregulation of several trafficking proteins, involved in vesicular exocytosis (Rab5B), synapse elimination (UBE3A), scission of endocytosis (DBN1), transport of ER in dendritic spines (MYO5A), presynaptic activity-dependent bulk endocytosis (FMR1), and NMDA receptor activity (GRIN2A). Chronic fluoxetine treatment of Ts65Dn mice rescued synaptic vesicular abnormalities and prevented abnormal proteomic changes in adult Ts65Dn mice, pointing to therapeutic targets for potential treatment of DS.
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    Potential Dextromethorphan-Induced Serotonin Syndrome Leading to Homicide and Suicide
    (Sage, 2024-01-30) Pavelka, Matthew M.; Kohr, Roland; Medicine, School of Medicine
    Limited case reports have been published regarding serotonin syndrome due to the combined effects of supratherapeutic levels of dextromethorphan and selective serotonin reuptake inhibitor. We report a case of an adolescent with postmortem findings suggestive of a diagnosis of serotonin syndrome-induced psychosis associated with a double homicide and suicide. Postmortem toxicology of the suicide victim was remarkable for elevated serotonergic metabolites of fluoxetine and dextromethorphan in a 14-year-old male.