• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Limbic Encephalitis Exacerbations and Remissions Charted by Microglial PET Scan: A Case Study (P4.104)
CONCLUSIONS: C-11-PK11195 PET imaging can be useful in the diagnosis of limbic encephalitis and for monitoring response to treatment. MALT lymphoma may also be associated with autoimmune or paraneoplastic encephalitis, especially in individuals with other predisposing factors to autoimmune disorders, such as Tourette’s and autoimmune thyroid disease. The reduction in microglial activity with both IVIG and anti-psychotics supports previous findings that anti-psychotics may act through anti-inflammatory pathways.Disclosure: Dr. Shatz has received research support from Janssen Pharmaceutica. Dr. Chugani has nothing to disclose.
Source: Neurology - April 8, 2015 Category: Neurology Authors: Shatz, R., Chugani, H. Tags: Aging, Dementia, Cognitive, and Behavioral Neurology: Rapidly Progressive and Inflammatory Dementias 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

Pages: 1  2  3