New Pathways to Parkinson’s and Alzheimer’s Diseases

Cohen & Oalican, LLP share recent Alzheimer's research.

Although Alzheimer's disease, Parkinson's disease and Huntington's disease have different genetic causes and pathways, all these ailments have one thing in common. All of them cause untimely death of the brain cells and the reason that this happens has been a dilemma to the treatment of these fatal diseases.

A recent study by a group of doctors and others at the Sanford-Burnham Medical Research Institute that was published in the July 30 issue of the medical journal Molecular Cell, throws some light on this brain cell death in patients of these diseases. The sudden and untimely transfer of a gaseous molecule called NO or nitric oxide from one cell protein to another could be the answer. Earlier research had revealed that NO and other molecules were responsible for nerve cell death or survival, but in this case, NO was seen to actually move from one protein to another through new molecular channels, triggering cellular suicide.

This was explained by the senior author of the research study group and the director of the Del E. Web Center for Neuroscience, Aging and Stem Cell Research at Sanford-Burnham, Stuart A. Lipton, M.D., Ph.D. Since this molecular evidence for the untimely cell death in Parkinson’s, Alzheimer's, and Huntington's diseases has been discovered, it would be possible now to utilize this new breakthrough to diagnose, treat and hopefully prevent these illnesses in the near future. As a Harvard-educated neurologist who runs his own clinical practice, Dr. Lipton is familiar with these fatal diseases as he observes his patients.

This research study has revealed that NO molecules relocate from the caspases to the XIAP proteins; the former are proteins that usually trigger cell death while the latter inhibit it. The caspases protein throws the NO molecule away like a “hot potato” to the XIAP protein to avoid the imminent cell death and this process happens through a chemical reaction called transnitrosylation. This action brings about a dual distress for the brain cells, as these cells are programmed to self-destruct when caspases do not have NO on them or XIAP have the molecule attached to them. Either way then it is death for the brain cells, as both these fatal actions happen simultaneously. In the study, it was shown that persons with neurodegenerative diseases had the NO molecule attached to the XIAP protein more frequently than those with normal brains. This reinforced the theory that this change in protein structure brings about cell degeneration.

The research group used a new arrangement of the Nernst equation to understand and analyze whether the caspases or the XIAP protein is more likely to end up with the NO molecule. The Nernst equation is taught in every chemistry class and is a mathematical equation that was found in the 19^th century. This possible prediction of the NO attachment to the brain cell proteins may ultimately help doctors to make earlier diagnosis of these neurodegenerative ailments, thereby kindling hope for treatment and cure. Cerebrospinal fluid and brain tissue from patients suffering from Parkinson's and Alzheimer’s is being studied and analyzed to find out whether the NO-attached proteins could be utilized as biomarkers to understand the progress and evolution of these diseases.

In ongoing research based on these findings, to formulate treatment and therapy to treat these neurodegenerative ailments, Dr. Lipton and his team are using robotic technology in Sanford-Burnham's Conrad Prebys Center for Chemical Genomics. Chemicals are being screened in their thousands to discover drugs that may stop the movement of the NO molecule from one protein to another, which may soon prevent brain cell death.

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