Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). In murine experimental encephalomyelitis (EAE) model MS, T regulatory (Treg) cell therapy has proved to be beneficial, but generation stable CNS-targeting Tregs needs further development. Here, we propose gene engineering achieve from naïve CD4 cells and demonstrate their efficacy in EAE model. CD4+ were modified utilizing a lentiviral vector express chimeric antigen receptor (CAR) targeting myelin...

The cyanobacterial toxin β-N-methylamino-l-alanine (BMAA) has been proposed to contribute neurodegenerative disease. We have previously reported a selective uptake of BMAA in the mouse neonatal hippocampus and that exposure during period causes learning memory impairments adult rats. aim this study was characterize effects brain 6-month-old rats treated neonatally (postnatal days 9–10) with glutamatergic BMAA. Protein changes were examined using novel technique Matrix-Assisted Laser...

Cyanobacteria are extensively distributed in terrestrial and aquatic environments all over the world. Most cyanobacteria can produce neurotoxin β-N-methylamino-L-alanine (BMAA), which has been detected several water systems could accumulate food chains. The aim of study was to investigate transfer BMAA fetal neonatal brains effects on development behavioral characteristics during brain growth spurt (BGS) rodents. Pregnant mice were given an injection 3H-BMAA gestational day 14 postnatal...

beta-N-methylamino-l-alanine (BMAA), a neurotoxic amino acid produced by cyanobacteria, has been suggested to be involved in the etiology of neurodegenerative disease complex which includes Parkinson-dementia (PDC). In PDC, neuromelanin-containing neurons substantia nigra are degenerated. Many PDC patients also have an uncommon pigmentary retinopathy. The aim this study was investigate distribution (3)H-BMAA mice and frogs, with emphasis on pigment-containing tissues. Using autoradiography,...

Most cyanobacteria (blue-green algae) can produce the neurotoxin β-N-methylamino-L-alanine (BMAA). Dietary exposure to BMAA has been suggested be involved in etiology of neurodegenerative disease amyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS/PDC). Little is known about BMAA-induced neurotoxicity following neonatal administration. Our previous studies have revealed an uptake hippocampus and striatum mice. Furthermore, rats treated with during period displayed acute but...

β-Methylamino-L-alanine (BMAA) is a non-proteinogenic amino acid that induces long-term cognitive deficits, as well an increased neurodegeneration and intracellular fibril formation in the hippocampus of adult rodents following short-time neonatal exposure vervet monkey brain exposure. It has also been proposed to be involved etiology neurodegenerative disease humans. The aim this study was identify metabolic effects not related excitotoxicity or oxidative stress human neuroblastoma SH-SY5Y...

The environmental neurotoxin β-N-methylamino-l-alanine (BMAA) has been implicated in the etiology of neurodegenerative disease, and recent studies indicate that BMAA can be misincorporated into proteins. is a developmental neurotoxicant induce long-term learning memory deficits, as well regionally restricted neuronal degeneration mineralization hippocampal CA1. aim study was to characterize changes (2 weeks 6 months) further brain adult rats treated neonatally (postnatal days 9–10) with (460...

Treatment with mesenchymal stromal cells (MSCs) is currently of interest for a number diseases including multiple sclerosis. MSCs are known to target inflamed tissues, but in therapeutic setting their systemic administration will lead few reaching the brain. We hypothesized that may brain upon intranasal and persist central nervous system (CNS) tissue if expressing CNS-targeting receptor. To demonstrate proof concept, were genetically engineered express myelin oligodendrocyte...

Concerns have been raised regarding the potential adverse health effects of ubiquitous herbicide glyphosate. Here, we investigated long-term developmental exposure to a glyphosate-based (GBH) by analyzing serum melatonin levels and cellular changes in striatum adult male rats (90 days old). Pregnant lactating were exposed 3% GBH (0.36% glyphosate) through drinking water from gestational day 5 postnatal 15. The offspring showed reduced (43%) at age compared with control group. perinatal also...

The cyanobacterial toxin β-N-methylamino-l-alanine (BMAA) is suggested to play a role in neurodegenerative disease. We have previously shown that although the selective uptake of BMAA rodent neonatal striatum does not cause neuronal cell death, exposure during development leads cognitive impairments adult rats. aim present study was characterize changes striatal neuropeptide systems male and female rat pups treated neonatally (postnatal days 9-10) with (40-460 mg/kg). label-free...

The cyanobacterial neurotoxin β-N-methylamino-L-alanine (BMAA) has been implicated in the etiology of neurodegenerative disease and proposed to be biomagnified terrestrial aquatic food chains. We have previously shown that neonatal period rats, which humans corresponds last trimester pregnancy first few years age, is a particularly sensitive for exposure BMAA. present study aimed examine secretion 14C-labeled L- D-BMAA into milk lactating mice subsequent transfer BMAA developing brain....

Abstract: In mice given a single intraperitoneal injection of the antithyroid drug methimazole (0.44 mmol/kg; 50 mg/kg) detachment olfactory neuroepithelium and necrosis Bowman’glands in lamina propria was observed 24 hr after administration. Three days administration there an atypical epithelium throughout region Bowman's glands had disappeared. Pretreatment with cytochrome P450 inhibitor metyrapone protected against methimazole‐induced changes at this site. injected analogues...

Immunohistochemistry and autoradiography were used to identify sites of the cytochrome P450 enzymes (P450) 1A1 1B1 expression activation 7,12-dimethylbenz(a)anthracene (DMBA), in brain rodents pretreated with aryl hydrocarbon receptor (AhR) agonists beta-naphthoflavone (BNF), 3,3',4,4',5-pentachlorobiphenyl or vehicle. revealed that CYP1A1 was preferentially induced endothelial cells (EC) choroid plexus, veins leptomeninges, cerebral AhR agonist-pretreated mice. No induction occurred...