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-dependent protease that exerts its effects through the proteolytic cleavage of target proteins.
Neuron-specific conditional deletions of calpain 1 and 2 impair long-term potentiation in the hippocampus and spatial learning.
Demonstrating corresponding biomarker and neurocognitive improvements will corroborate results, and may facilitate more tailored treatment approaches in the future.
Deidentified data will be entered into the Federal Interagency TBI Research Informatics System (FITBIR) through the CNRM after completion of the study and after all codes or links to personal identifying information have been destroyed.
Moreover, recent studies have suggested distinct roles of calpain 1 and 2 in synaptic plasticity.
However, the role of hippocampal calpain in memory processes, especially memory consolidation, reconsolidation, and extinction, is still unclear.
RTM was first used to treat phobias in the 1970s, and has more recently been refined to focus on reconsolidation to update long-term memories, reconfiguring the salience structure of the original memory, and incorporating those changes into the overall memory structure.
Reconsolidation is a neural mechanism for updating long-term memory, inserting new information that contradicts an essential element of the memory, which makes it possible to change the emotional tone and salience of the memory.More palatable and effective therapies for PTSD, with and without TBI, must be developed and evaluated.