The finding that Cdk5 inhibition can convert LTD-dominant striatal plasticity to LTP represents a potentially novel therapeutic target. However, the downstream signaling pathways and molecular switches that enable this plasticity reversal remain unexplained, limiting translational potential. Gap type: unexplained_observation Source paper: Exploring the role of Cdk5 on striatal synaptic plasticity in a 3-NP-induced model of early stages of Huntington's disease. (2024, Frontiers in molecular neuroscience, PMID:39569019)
Landscape Summary: What molecular mechanisms allow Cdk5 inhibition to unmask LTP in striatal neurons during early neurodegeneration? is a 0.82 priority gap in synaptic-biology. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
What molecular mechanisms allow Cdk5 inhibition to unmask LTP in striatal neurons during early neurodegeneration? — INVOKE-2 (completed)
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