Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038220 (status epilepticus)
7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ATP is a (co)transmitter and signaling molecule in the CNS. It acts at a multitude of ligand-gated cationic channels termed P2X to induce rapid depolarization of the cell membrane. Within this receptor-channel family, the P2X7 receptor (R) allows the transmembrane fluxes of Na⁺, Ca²⁺, and K⁺, but also allows the slow permeation of larger organic molecules. This is supposed to cause necrosis by excessive Ca²⁺ influx, as well as depletion of intracellular ions and metabolites. Cell death may also occur by apoptosis due to the activation of the caspase enzymatic cascade. Because P2X7Rs are localized in the CNS preferentially on microglia, but also at a lower density on neuroglia (astrocytes, oligodendrocytes) the stimulation of this receptor leads to the release of neurodegeneration-inducing bioactive molecules such as pro-inflammatory cytokines, chemokines, proteases, reactive oxygen and nitrogen molecules, and the excitotoxic glutamate/ATP. Various neurodegenerative reactions of the brain/spinal cord following acute harmful events (mechanical CNS damage, ischemia, status epilepticus) or chronic neurodegenerative diseases (neuropathic pain, Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis) lead to a massive release of ATP via the leaky plasma membrane of neural tissue. This causes cellular damage superimposed on the original consequences of neurodegeneration. Hence, blood-brain-barrier permeable pharmacological antagonists of P2X7Rs with excellent bioavailability are possible therapeutic agents for these diseases. The aim of this review article is to summarize our present state of knowledge on the involvement of P2X7R-mediated events in neurodegenerative illnesses endangering especially the life quality and duration of the aged human population.
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PMID:P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases. 3282 23

The high-fat, low-carbohydrate ketogenic diet (KD) is an established treatment for drug-resistant epilepsy with a proven efficacy. The KD is being explored for Febrile Infection-Related Epilepsy Syndrome (FIRES) and epileptic encephalopathies. There is growing evidence that KD works by targeting dysregulated adaptive and innate immunity that occurs in drug-resistant epilepsy and in refractory status epilepticus. Beyond epilepsy, there are yet additional potential uses in neurological disorders because KD appears to have the broad anti-inflammatory and neuroprotective properties. The KD exerts anti-inflammatory action against a variety of experimental models of neurological disorders including multiple sclerosis, Parkinson's disease, pain, and spinal cord injury. Anti-inflammatory action of KD appears to be mediated by multiple mechanisms. Ketones bodies, caloric restriction, polyunsaturated fatty acids and gut microbiota modifications might be involved in the modulation of inflammation by the KD.
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PMID:Ketogenic diet and Neuroinflammation. 3298 44

SUMMARYHuman herpesvirus 6A (HHV-6A) and human herpesvirus 6B (HHV-6B), collectively termed HHV-6A/B, are neurotropic viruses that permanently infect most humans from an early age. Although most people infected with these viruses appear to suffer no ill effects, the viruses are a well-established cause of encephalitis in immunocompromised patients. In this review, we summarize the evidence that the viruses may also be one trigger for febrile seizures (including febrile status epilepticus) in immunocompetent infants and children, mesial temporal lobe epilepsy, multiple sclerosis (MS), and, possibly, Alzheimer's disease. We propose criteria for linking ubiquitous infectious agents capable of producing lifelong infection to any neurologic disease, and then we examine to what extent these criteria have been met for these viruses and these diseases.
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PMID:Human Herpesviruses 6A and 6B in Brain Diseases: Association versus Causation. 3317 86


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