Glutamate Excitotoxicity and Neurodegeneration
نویسندگان
چکیده
منابع مشابه
Glutamate/NMDA excitotoxicity and HMGB1/TLR4 neuroimmune toxicity converge as components of neurodegeneration
Neurodegeneration in brain is linked to both excitotoxicity and neuroimmune gene induction, although the mechanisms are poorly understood. High-mobility group box 1 (HMGB1) is a cytokine like molecule released in brain by glutamate that has been found to enhance neuronal excitability through Toll-like receptor 4 (TLR4). To explore the role of HMGB1 in glutamate/NMDA excitotoxicity or neuroimmun...
متن کاملOncogene AEG-1 promotes glioma-induced neurodegeneration by increasing glutamate excitotoxicity.
Aggressive tumor growth, diffuse tissue invasion, and neurodegeneration are hallmarks of malignant glioma. Although glutamate excitotoxicity is considered to play a key role in glioma-induced neurodegeneration, the mechanism(s) controlling this process is poorly understood. Astrocyte elevated gene-1 (AEG-1) is an oncogene that is overexpressed in several types of human cancers, including more t...
متن کاملThe role of excitotoxicity in neurodegeneration.
A body of evidence suggests that the mechanisms of excitotoxic neuronal damage evoked by excessive or prolonged activation of the excitatory amino acid receptors may be involved in pathogenesis of brain damage in acute insults and in chronic neurodegenerative diseases. In this review we briefly discuss several selected mechanisms of the excitotoxicity, focusing attention on the role of ionotrop...
متن کاملCholesterol loss during glutamate-mediated excitotoxicity.
The deregulation of brain cholesterol metabolism is typical in acute neuronal injury (such as stroke, brain trauma and epileptic seizures) and chronic neurodegenerative diseases (Alzheimer's disease). Since both conditions are characterized by excessive stimulation of glutamate receptors, we have here investigated to which extent excitatory neurotransmission plays a role in brain cholesterol ho...
متن کاملInflammatory neurodegeneration mediated by nitric oxide from activated glia-inhibiting neuronal respiration, causing glutamate release and excitotoxicity.
Glia undergo inflammatory activation in most CNS pathologies and are capable of killing cocultured neurons. We investigated the mechanisms of this inflammatory neurodegeneration using a mixed culture of neurons, microglia, and astrocytes, either when the astrocytes were activated directly with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) or LPS/IFN-gamma-activated microglia were ad...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Molecular and Genetic Medicine
سال: 2014
ISSN: 1747-0862
DOI: 10.4172/1747-0862.1000141