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Arterial Spin Labeling Imaging Characteristics of Anti-leucine-rich Glioma-Inactivated 1 Encephalitis: A Qualitative and Quantitative Analysis
DiscussionIn this preliminary study of six patients, we demonstrate an ASL hyperperfusion pattern, with a possible predilection for the right mesial temporal lobe on both qualitative and quantitative assessments in patients with seropositive LGI1. Larger scale studies are necessary to further characterize the strength of these associations.
Source: Frontiers in Neurology - July 28, 2022 Category: Neurology Source Type: research

The Expression and Significance of the Plasma Let-7 Family in Anti- N -methyl- d -aspartate Receptor Encephalitis
Abstract The study aimed to investigate the expression and significance of the plasma let-7 family in anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis. Blood samples from 5 anti-NMDAR encephalitis patients and 5 negative controls were collected for microarray analysis. Blood samples from10 anti-NMDAR encephalitis patients, 10 anti-NMDAR encephalitis patients whose physical conditions have improved after 3 months of immunotherapy, 20 virus (meningitis) encephalitis patients, 20 tuberculosis (meningitis) encephalitis patients, 10 purulent (meningitis) encephalitis patients, 20 cerebral cysticercosis patient...
Source: Journal of Molecular Neuroscience - June 23, 2015 Category: Neuroscience Source Type: research

GLUTAMATE RECEPTOR ANTIBODIES IN NEUROLOGICAL DISEASES: Anti-AMPA-GluR3 antibodies, Anti-NMDA-NR1 antibodies, Anti-NMDA-NR2A/B antibodies, Anti-mGluR1 antibodies or Anti-mGluR5 antibodies are present in subpopulations of patients with either: Epilepsy, Encephalitis, Cerebellar Ataxia, Systemic Lupus Erythematosus (SLE) and Neuropsychiatric SLE, Sjogren's syndrome, Schizophrenia, Mania or Stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor's expression, impair glutamate-induced signaling and function, activate Blood Brain Barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and Ataxia in animal models, and can be removed or silenced in some patients by immunotherapy.
Abstract Glutamate is the major excitatory neurotransmitter of the Central Nervous System (CNS), and it is crucially needed for numerous key neuronal functions. Yet, excess glutamate causes massive neuronal death and brain damage by excitotoxicity-detrimental over activation of glutamate receptors. Glutamate-mediated excitotoxicity is the main pathological process taking place in many types of acute and chronic CNS diseases and injuries. In recent years, it became clear that not only excess glutamate can cause massive brain damage, but that several types of anti-glutamate receptor antibodies, that are present in ...
Source: Herpes - August 1, 2014 Category: Infectious Diseases Authors: Levite M Tags: J Neural Transm Source Type: research