ReviewMolecular neurobiology2026
RTK-PI3K/Akt Signaling in the Hippocampus: A Key Regulator of Structural Synapse Remodeling and Degeneration.
Review in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
One of the main morphological manifestations of synaptic plasticity is structural synaptic remodeling, where LTP and LTD cause activity-dependent modifications in the creation, development, maturation, stability, and removal of dendritic spines. RTK-mediated PI3K/Akt signaling is crucial for controlling various structural modifications in the hippocampus, such as the formation of filopodia and dendritic spine maturation. Crosstalk with other signaling pathways such as mTORC1, GSK3β, and Wnt modifies structure and improves synaptic plasticity by increasing the expression of AMPAR and its stability and lowering endocytosis. Dysregulation of PI3K/Akt signaling, including both insufficient and excessive pathway activation, may disturb spine remodeling and synaptic homeostasis in neurological disorders. Short-term inhibition of the pathway helps in maturation of the spine, but sustained activation promotes dendritic protrusion growth rather than maturation. That may lead to improper development of dendritic spines, which further compromises synaptic transmission and synaptic plasticity. Precise spatiotemporal and cell-type-specific modulation of PI3K/Akt signaling may offer therapeutic opportunities, although major experimental and translational challenges remain.
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