How the Wnt signaling pathway protects from neurodegeneration: The mitochondrial scenario

摘要: Alzheimer's disease (AD) is the most common neurodegenerative disorder and characterized by progressive memory loss cognitive decline. One of hallmarks AD overproduction amyloid-beta aggregates that range from toxic soluble oligomer (Aβo) form to extracellular accumulations in brain. Growing evidence indicates mitochondrial dysfunction a feature diseases observed at an early stage pathogenesis AD. Reports indicate structure function are affected Aβo can trigger neuronal cell death. Mitochondria highly dynamic organelles, balance between their fusion fission processes essential for function. Interestingly, AD, process known as "mitochondrial dynamics" also impaired Aβo. On other hand, activation Wnt signaling pathway has role synaptic maintenance functions, its deregulation been implicated We have demonstrated canonical signaling, through Wnt3a ligand, prevents permeabilization membranes inhibition permeability transition pore (mPTP), induced In addition, we showed non-canonical Wnt5a protects mitochondria fission-fusion alterations These results suggest new approaches which different pathways protect neurons support idea become potential therapeutic targets treatment disorders. Here discuss neuroprotective differential modulation processes, associated with neurodegeneration.