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Blocking Dkk-1 suppresses β-amyloid peptide-induced neuronal synapse loss in transgenic mouse models of Alzheimer’s disease.

Alzheimer’s disease (AD) is characterized by synaptic dysfunction, early loss of synapses and progressive accumulation of β-amyloid peptide aggregates, leading to cognitive dysfunction. Soluble oligomeric forms of β-amyloid decrease the number and strength of synapses prior to neuronal cell death. It appears that β-amyloid causes synaptic loss through the deregulation of Wnt proteins, which are known to promote synapse formation and maintenance. A variant of the low-density lipoprotein receptor-related protein 6 (LRP6), a co-receptor in the canonical Wnt pathway, is associated with late-onset AD and this variant results in low levels of Wnt signaling. Dr. Patricia Salinas and colleagues at the University College London demonstrated that acute exposure to β-amyloid oligomers induces Dickkopf-1 (Dkk-1) expression together with the loss of synaptic sites (Purro et al (2012) J Neurosci. 32(10):3492-8). They further found that Dkk1-neutralizing antibodies suppress β-amyloid -induced loss of synapses in mouse brain slices. The highlighted research establishes that Dkk-1 mediates β-amyloid-induced synapse disassembly and further suggests that Dkk-1 inhibition might be therapeutically beneficial for the maintenance of synapses, which in turn could prevent cognitive decline in AD.

Over the past ten years, Enzo scientists and collaborators have made significant contributions to the understanding of the canonical Wnt/β–Catenin pathway, as demonstrated by our peer-reviewed publications and intellectual property. We further extend our commitment to progress in this scientific field by offering assays and reagents that we have developed and ourselves use, to the broader research community.


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