Researchers have provided new information about how communication among neurons may be prevented from deteriorating in conditions such as Alzheimer's disease (AD). The new results may lead to new therapies for the treatment of not only AD but also motor neuron diseases and prion diseases.
Most current research efforts to find a treatment for AD and similar conditions focuses on what happens to the main part -- or body -- of a neuron, but recent studies have examined how neuronal communication is impaired in human diseases such as AD. When a neuron interacts with another neuron, it uses an extension called an axon that releases chemicals, which diffuse across a tiny gap between the neurons called a synapse and crosses the other neuron.
Deterioration of synapses and axons can be delayed thanks to a protein created by a gene called the slow Wallerian degeneration (Wlds) gene. How this protein works is still a mystery, but it may lead to new therapies for the treatment of AD and other conditions.
Thomas H. Gillingwater and colleagues identified 16 proteins that are affected by the Wlds gene. Although details are still missing, Wlds probably prevents these proteins from deteriorating synapses and axons.
The scientists found that some of the proteins had previously been shown to deteriorate synapses and axons, but, unexpectedly, eight proteins regulate the function of mitochondria -- cellular organelles that supply energy to cells. These results reveal for the first time that mitochondria are involved in the protection of neurons provided by the Wlds gene and suggest that targeting some of the proteins identified in this study may lead to novel therapies for the treatment of AD, motor neuron diseases, and prion diseases.
Article: "Differential proteomic analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene," by Thomas M. Wishart, Janet M. Paterson, Duncan M. Short, Sara Meredith, Kevin A. Robertson, Calum Sutherland, Michael A. Cousin, Mayank B. Dutia, and Thomas H. Gillingwater
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