منابع مشابه
Prions can infect primary cultured neurons and astrocytes and promote neuronal cell death.
Transmissible spongiform encephalopathies arise as a consequence of infection of the central nervous system by prions, where neurons and glial cells are regarded as primary targets. Neuronal loss and gliosis, associated with the accumulation of misfolded prion protein (PrP), are hallmarks of prion diseases; yet the mechanisms underlying such disorders remain unclear. Here we introduced a cell s...
متن کاملP3: Neuronal Death Following Posttraumatic Excitability and Seizure
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متن کاملNeuronal injury and death following focal mild brain injury: The role of network excitability and seizure
Objective(s): While traumatic brain injury (TBI) is a predisposing factor for development of post-traumatic epilepsy (PTE), the occurrence of seizures following brain trauma can infuriate adverse consequences of brain injury. However, the effect of seizures in epileptogenesis after mild TBI cannot yet be accurately confirmed. This study was designed to investigate the ...
متن کاملp3: neuronal death following posttraumatic excitability and seizure
seizure may occur after mild traumatic brain injury (tbi), and the severity of tbi can be considered the most crucial factor for an increased risk of recurring seizures as well as for the development of posttraumatic epilepsy. however, the effect of seizures in epileptogenesis after mild tbi cannot yet be accurately confirmed. this study was designed to determine whether mild tbi increases seiz...
متن کاملNeuronal Cell Death
penheim, 1991; Burek and Oppenheim, 1998). Although Neurons may die at many different developmental stages some of these hypotheses have received experimental and for many different reasons. As in other tissues, difsupport in individual systems, none seems to be generferent stimuli produce quite different morphological ally applicable. Indeed, it remains to be demonstrated that manifestations o...
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ژورنال
عنوان ژورنال: Cell Death & Disease
سال: 2010
ISSN: 2041-4889
DOI: 10.1038/cddis.2009.9