Abstract
It is well recognized the role of the Wnt pathway in many developmental processes such as neuronal maturation, migration, neuronal connectivity and synaptic formation. Growing evidence is also demonstrating its function in the mature brain where is associated with modulation of axonal remodeling, dendrite outgrowth, synaptic activity, neurogenesis and behavioral plasticity. Proteins involved in Wnt signaling have been found expressed in the adult hippocampus suggesting that Wnt pathway plays a role in the hippocampal function through life. Indeed, Wnt ligands act locally to regulate neurogenesis, neuronal cell shape and pre- and postsynaptic assembly, events that are thought to underlie changes in synaptic function associated with long-term potentiation and with cognitive tasks such as learning and memory. Recent data have demonstrated the increased expression of the Wnt antagonist Dickkopf-1 (DKK1) in brains of Alzheimer´s disease (AD) patients suggesting that dysfunction of Wnt signaling could also contribute to AD pathology. We review here evidence of Wnt-associated molecules expression linked to physiological and pathological hippocampal functioning in the adult brain. The basic aspects of Wnt related mechanisms underlying hippocampal plasticity as well as evidence of how hippocampal dysfunction may rely on Wnt dysregulation is analyzed. This information would provide some clues about the possible therapeutic targets for developing treatments for neurodegenerative diseases associated with aberrant brain plasticity.
Highlights
The mature brain undergoes continuous morphological changes in response to external and internal stimuli through the turnover and reorganization of neuronal networks and synapses [1,2,3]
All signaling events implicated in the Wnt pathway must occur in a coordinate fashion so synaptic contacts remain dynamic in the adult brain allowing a continuous fine balance between synaptic formation and synapse disassembly [5]
Studies on the relationships between Wnt/ catenin pathway and spatial memory have described that the expression of the calcium/calmodulin-dependent protein kinase type IV (CaMKIV) is modulated by Wnt3a and that the administration of lithium restores the levels of CaMKIV and improves the spatial memory deficits in a transgenic model of Alzheimers disease (AD) [77]
Summary
The mature brain undergoes continuous morphological changes in response to external and internal stimuli through the turnover and reorganization of neuronal networks and synapses [1,2,3]. The specific pattern of genes encoding Wnt ligands, receptors, and inhibitory proteins reported in the adult hippocampus evidences the potential role for Wnt signaling in broad hippocampal functions.
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