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"Enhance brain plasticity" refers to amplifying the capacity of the brain to reorganize and form new neural connections, critical for learning, memory, adaptation to injury, and recovery from neurological and psychiatric disorders[7][2][4]. This is achieved through a coordinated interplay of molecular pathways involving neurotrophic factors (most notably brain-derived neurotrophic factor, BDNF, and its receptor TrkB), neurotransmitter receptor regulation (such as glutamatergic NMDA and AMPA receptors), intracellular signaling cascades (including CaMKII, PKA), and changes in gene expression leading to synaptic remodeling[1][3][6][5]. Neuroplasticity-enhancing strategies play a key therapeutic role in conditions such as depression, neurodegenerative diseases, and recovery from brain injury, often targeted indirectly by drugs or neurostimulatory approaches[4][2][5]. In summary, "Enhance brain plasticity" is a therapeutic strategy or effect, not a molecule or receptor; it covers a molecularly diverse and complex landscape. For structured data, the particular molecule or pathway (e.g., BDNF, TrkB receptor, NMDA receptor) should be specified for full canonical target information[1][3][6][5].
Modulation of neurotrophic signaling (e.g., BDNF-TrkB pathway); Enhancement of synaptic transmission (e.g., via NMDA receptor or AMPA receptor upregulation); Activation of intracellular kinase cascades (e.g., CaMKII, PKA); Epigenetic changes and altered gene expression
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