Scientists at Harvard Medical School have found that the hypersensitive and sensitive neurons of the cephaplod nervous systems of vertebrates and fish, the main sources of damage to their nervous systems, are genetically different.
This finding is a major step toward understanding how some neurodegenerative diseases such as Alzheimer’s and Parkinson’s affect brain function and cognition.
The findings, published in Nature, are important for understanding how a common neurological disease may be inherited in a way that can be passed on to offspring, said co-author of the paper, Eric Stutz, PhD, associate professor of molecular and cell biology.
The researchers, led by Dr. Stutz and a research assistant, looked at the gene encoding the hypersensitivity gene in vertebrates, fish and humans.
They found that, unlike mammals and some insects, the gene is not only expressed in the brain but also in the spinal cord, which plays a crucial role in regulating the body’s energy-flow to and from the body.
This discovery could lead to the development of novel drugs to treat the disorder.
“We think this is going to help us develop new treatments for this disorder,” Dr. Dracele said.
“The most exciting part is that we now know that this gene is involved in both the neural system and the nervous system,” he said.
The hypersensitive gene is located in a region of the genome called the X chromosome, which has been linked to many other genetic disorders.
The researchers have previously found that certain other genes are involved in the development and function of the nervous systems.
For example, genes encoding a type of protein called neuropeptide Y, which regulates neurotransmitter levels in the nervous cells, are also involved in regulating activity of the hypersensitised neurons.
The authors speculate that, in the absence of a hypersensitive neuron, the brain would be starved of these neurotransmitters, which may lead to a cascade of neurodegenesis.
“These genes are essential for normal brain function.
This means that they are critical to the survival of nervous systems in general,” Draceles said.
Scientists previously thought that the genes that encode the hypersense proteins were the same genes that cause hypersensitivity in vertebrate animals, including mice, and that they were involved in a number of neurological disorders.
“Our finding that they differ is a new result that is a very exciting development,” Drcele said, adding that the research team is now trying to understand how other genes that control different functions of the neurons are also expressed in fish and mammals.
“We are hopeful that we can now identify a way to use this information to target these genes in other animals, which could lead us to develop new drugs for neurological diseases,” Dradele said.
“In humans, a hypersensitivity disorder affects about 20 percent of the population, and it is not clear whether it is caused by a common genetic disorder or by a combination of genetic and environmental factors, Dracels said.
In addition to Dracells and Draceletts, co-authors on the paper are: Yilun Wu, PhD; Michael H. Siegel, PhD.