Ca 2+ Signals and Neuronal Death in Brain Ischemia

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Ca Signals and Neuronal Death in Brain Ischemia

Although Ca signals are necessary for cell communication and survival, abnormal cellular Ca load can trigger different cell death programs. Ca mediates cell death by activating proteases (ie, calpains), by reinforcing signals leading to caspase activation or by triggering other catabolic processes mediated by lipases and nucleases. Failure in the clearance of excitatory amino acid is a critical...

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Ca2+ signals and neuronal death in brain ischemia.

Although Ca(2+) signals are necessary for cell communication and survival, abnormal cellular Ca(2+) load can trigger different cell death programs. Ca(2+) mediates cell death by activating proteases (ie, calpains), by reinforcing signals leading to caspase activation or by triggering other catabolic processes mediated by lipases and nucleases. Failure in the clearance of excitatory amino acid i...

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Phagocytosis executes delayed neuronal death after focal brain ischemia.

Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood. Phagocytic removal of neurons is generally assumed to be beneficial and to occur only after neuronal death. However, we report herein that inhibition of phagocytosis can prevent delayed loss and death of functional neurons after transient brain i...

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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 ...

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ژورنال

عنوان ژورنال: Stroke

سال: 2007

ISSN: 0039-2499,1524-4628

DOI: 10.1161/01.str.0000256294.46009.29