Researchers at the Boyce Thompson Institute and John Hopkins University discovered that salicylic acid, the primary breakdown product of aspirin, binds to the enzyme GAPDH (Glyceraldehyde 3-Phosphate Dehydrogenase), thereby stopping it from moving into a cell’s nucleus. The anti-Parkinson’s drug deprenyl blocks GAPDH’s entry into the nucleus and the resulting cell death. The researchers discovered that salicylic acid also is effective at stopping GAPDH from moving into the nucleus and preventing cell death. This study also suggests that derivatives of salicylic acid may hold promise for treating Alzheimer’s disease.
Daniel Klessig is the senior author of that study and is a professor at Boyce Thompson Institute and Cornell University. He has mainly studied the effects and actions of salicylic acid in plants. Salicylic acid is the critical hormone for regulating the plant’s immune system.
In the new study, the researchers performed high-throughput screens to identify proteins in the human body that bind to salicylic acid. GAPDH is a central enzyme in glucose metabolism, but plays additional roles in the cell. Under oxidative stress—an excess of free radicals and other reactive compounds—GAPDH is modified and then enters the nucleus of neurons, where it enhances protein turnover, leading to cell death.
Co-author Solomon Snyder, professor of neuroscience at Johns Hopkins University in Baltimore said, “The new study establishes that GAPDH is a target for salicylate drugs related to aspirin, and hence may be relevant to the therapeutic actions of such drugs.”
This can potentially be an enormous breakthrough for scientists everywhere looking to help treat certain neurodegenerative diseases such as Alzheimer’s. Who would have known, everyday aspirin can help with the treatment of Alzheimer’s disease?
To read the full study please visit the journal PLOS ONE