Sanford Burham logoThe genetic basis for Alzheimer’s disease, Parkinson’s disease and Huntington’s disease is believed to be different. But all the three disorders may be significantly described as the untimely death of brain cells. Scientists have for long tried to figure out what causes cell death in the brain. Well this article may help investigators to ascertain accurate treatments. A latest research conducted by the experts from the Sanford-Burnham Medical Research Institute (Sanford-Burnham) suggests that in some cases the reason is the inappropriate transfer of a gaseous molecule called as nitric oxide, or NO from one protein to another.

Researchers claim to have laid hands on NO-like molecules that are transferred from caspases, proteins which usually trigger cell death. These molecules are seemingly transferred to XIAP that is a protein generally known to restrict cell death. This entire process is assumed to be the result of transnitrosylation which is a chemical reaction.

Stuart A. Lipton, M.D., Ph.D., senior author of the research and director of the Del E. Web Center for Neuroscience, Aging and Stem Cell Research at Sanford-Burnham highlighted, “We and other researchers have shown that NO and related molecules can contribute to either nerve cell death or nerve cell survival. However, these new findings reveal that NO can actually jump from one protein to another in molecular pathways that lead to cellular suicide. Now that we have this molecular clue to the cause of nerve cell death in Parkinson’s, Alzheimer’s, and Huntington’s diseases, we can figure out how to use it to better diagnose and treat these diseases.”

A double whammy situation is apparently suffered by the brain when XIAP is holding NO. The situation is created probably because cells are programmed to self-destruct when XIAP has NO attached to it or when caspases don’t. So both brain cell-destroying events possibly take place together. More events of XIAP holding the NO were registered in patients with neurodegenerative diseases as compared to normal brains. This identification probably enabled researchers to conclude that protein modification causes cell damage.

Dr. Lipton commented, “We are currently analyzing cerebrospinal fluid and brain tissue from Parkinson’s, Alzheimer’s and other patients to determine if we can use the NO-tagged proteins as biomarkers for the disease.”

In order to ascertain the exact protein that may result in the NO ‘hot potato,’ caspases or XIAP, the scientists developed a latest version of the Nernst equation. Anticipating the precise protein can supposedly empower physicians to diagnose neurodegenerative disorders like Parkinson’s or Alzheimer’s disease in the early stages itself.

The scientists further aim to identify potential therapies for treating Parkinson’s, Alzheimer’s and Huntington’s diseases. Robotic technology has been employed to screen various chemicals as appropriate medications avoiding abnormal or extreme transfer of NO from one protein to another. So nerve cell injury and death can be safeguarded.

The research is published in the July 30 issue of Molecular Cell.