Background: Aprepitant (APR), a neurokinin 1 receptor antagonist, is an approved drug for treating chemotherapy-induced nausea and vomiting.
Objectives: Investigate the beneficial roles of APR alone or in combination with sodium valproate (VPA) against lithium pilocarpine [li-pilo]-induced seizures, behavioral changes, and cognitive deficits.
Methods: Thirty male mice were divided into five groups, each containing 6. "Vehicle Group I," "Control Group II "li-pilo, " Valproate (VPA) group III (400 mg/kg/i.p.), "APR group IV, " and "Combination Group V." Videos of mice were recorded, and they were watched for episodes of spontaneous recurring seizures (SRS). Behavioral Tests were performed. At the end of the study, animal brains were taken for biochemical assays and gene expression studies.
Results: APR partially protected against SRS with partial restoration of average behavioral and standard cognitive skills associated with a significant increase in brain SOD activity and a significant decrease in MDA, IL-1β, NF-КB, and SP-3 levels in relation to the control group. Interestingly, a combination of APR with VPA in epileptic mice showed complete protection against li-pilo-induced behavioral changes and cognitive deficits, a significant increase in brain SOD activity, and a considerable decrease in MDA, IL-1β, NF-ΚB, and SP levels to normal.
Conclusion: Using APR as an adjuvant to VPA is more effective in protecting against li-pilo-induced seizures, behavioral changes, and cognitive deficits due to its antioxidant, anti-inflammatory, and NK1 antagonist effects than using APR alone as drug therapy.
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http://dx.doi.org/10.1016/j.yebeh.2024.110028 | DOI Listing |
Case Rep Genet
January 2025
Medical Investigation of Neurodevelopmental Disorders (MIND) Institute, University of California, 2825 50th Street, Davis, Sacramento 95817, California, USA.
Fragile X syndrome (FXS) presents with autism spectrum disorder (ASD), intellectual disability, developmental delay, seizures, hypotonia during infancy, joint laxity, behavioral issues, and characteristic facial features. The predominant mechanism is due to CGG trinucleotide repeat expansion of more than 200 repeats in the 5'UTR (untranslated region) of (Fragile X Messenger Ribonucleoprotein 1) causing promoter methylation and transcriptional silencing. However, not all patients presenting with the characteristic phenotype and point/frameshift mutations with deletions in have been described in the literature.
View Article and Find Full Text PDFJ Community Hosp Intern Med Perspect
November 2024
Department of Internal Medicine, HCA Healthcare, MountainView Hospital, 2880 N Tenaya Way, 89128, Las Vegas, NV, USA.
Paraneoplastic limbic encephalitis (PLE) is a poorly understood condition, thought to be caused by the cross-reacting of tumor antibodies with neurons in the brain, resulting in neuropsychiatric sequelae, such as personality and behavioral changes, psychosis, memory loss, and seizures. Anti-contactin-associated protein-like 2 (CASPR2) antibodies can cause PLE in patients with particular tumors, which in most cases can be identified as thymoma, lung cancer, or endometrial cancer. Some case reports show rare instances with other tumors, such as throat or sigmoid carcinoma.
View Article and Find Full Text PDFMol Cell Pediatr
January 2025
Division of Metabolism and Children`s Research Center, University Children's Hospital Zurich, Lenggstr. 30, 8008, Zurich, Switzerland.
Background: Cerebral creatine deficiency disorders (CCDD) are rare diseases caused by defects in the enzymes L-arginine: glycine amidinotransferase (AGAT) or guanidinoacetate-N-methyltransferase (GAMT), which are involved in synthesis of creatine; or by a defect in the creatine transporter (CRTR), which is essential for uptake of creatine as important energy source into the target cells. Patients with CCDD can present with a variety of unspecific symptoms: global developmental delay, speech-language disorder, behavioral abnormalities and seizures. Early treatment initiation is essential in AGAT and GAMT deficiencies to achieve a favorable outcome.
View Article and Find Full Text PDFNeuron
January 2025
Department of Pathology and Cell Biology, Irving Cancer Research Center, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Neurological Surgery, Columbia University Irving Medical Center, New York, NY 10032, USA. Electronic address:
Gliomas are aggressive neoplasms that diffusely infiltrate the brain and cause neurological symptoms, including cognitive deficits and seizures. Increased mTOR signaling has been implicated in glioma-induced neuronal hyperexcitability, but the molecular and functional consequences have not been identified. Here, we show three types of changes in tumor-associated neurons: (1) downregulation of transcripts encoding excitatory and inhibitory postsynaptic proteins and dendritic spine development and upregulation of cytoskeletal transcripts via neuron-specific profiling of ribosome-bound mRNA, (2) marked decreases in dendritic spine density via light and electron microscopy, and (3) progressive functional alterations leading to neuronal hyperexcitability via in vivo calcium imaging.
View Article and Find Full Text PDFPediatr Neurol
December 2024
Department of Pediatrics, McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth) and Children's Memorial Hermann Hospital, Houston, Texas.
Background: Tuberous sclerosis complex (TSC) is a multisystemic genetic disorder with clinical variability. As the needs of children with TSC may differ, parenting demands may similarly differ. Characterizing parenting stress, or emotional maladaptation from parenting duties, can enable health care providers to assist parents of children with TSC.
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