Aspirin Component Combats Neurodegenerative Disorders

By Jonathan Springston, Associate Managing Editor, AHC Media

A study published this week reveals a component of aspirin could help scientists in the ongoing war on neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease.

Researchers from the Boyce Thompson Institute for Plant Research and Johns Hopkins University found that salicylic acid, the primary breakdown product of aspirin, binds to Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH), an enzyme pegged as a contributor to many neurodegenerative diseases. The salicylic acid acts as a firewall that can prevent GAPDH from entering a cell’s nucleus, which causes cell death.

“The enzyme GAPDH, long thought to function solely in glucose metabolism, is now known to participate in intracellular signaling,” co-author Solomon Snyder, professor of neuroscience at Johns Hopkins University in Baltimore, said in a statement. “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.”

Neurodegenerative disorders, particularly Alzheimer’s disease, are a frequent topic of discussion in AHC Media publications, particularly how alternative and natural treatments might prevent and combat such disorders.

In the Nov. 30 issue of Internal Medicine Alert, contributor Joseph Scherger, MD, MPH, wrote about the negative effects an unhealthy diet has on cognitive ability. And in the Nov. 15 issue, Dr. Scherger outlined how adherence to the Mediterranean diet improves cognitive ability.

In the October issue of Integrative Medicine Alert, Editor David Kiefer, MD, examined a study that found supplemental omega-3 fatty acids failed to find benefit on cognitive function over 5 years.

In the December issue of Neurology Alert, contributor Claire Henchcliffe, MD, discovered a study that demonstrated at postmortem that, in addition to dopaminergic deficits, the serotonergic and noradrenergic systems are profoundly disrupted in Parkinson’s disease patients with dementia when compared with normal controls. “The finding of deficits in these neurotransmitter systems in neocortical and limbic, as well as basal ganglia regions, serves to emphasize that a reliance on treatment strategies that focus on dopamine supplementation alone are simply inadequate in late stages of disease, aligning well with current clinical strategies,” she wrote.