New research highlights how nerves – whether harmed by disease or traumatic injury – start to die, a discovery that unveils novel targets for developing drugs to slow or halt devastating neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and amyolateral sclerosis as well as peripheral nerve damage.
Although peripheral neuropathies afflict some 20 million Americans, their underlying causes are not completely understood. Now, scientists have shown that damage to energy factories in Schwann cells, which grow alongside neurons and enable nerve signals to travel from the spinal cord to the tips of the fingers and toes, may play a central role. Shown is a Schwann cell surrounding nerve axons, shown in green.
The body’s ability to perform simple tasks like flex muscles or feel heat, cold and pain depends, in large part, on myelin, an insulating layer of fats and proteins that speeds the propagation of nerve cell signals. Now, scientists have identified a gene in mice that controls whether certain cells in the peripheral nervous system can make myelin. Called Gpr126, the gene encodes a cellular receptor that could play a role in diseases affecting peripheral nerves.