A new study reveals a possible "missing link" between over-stimulated neurons and neurodegenerative symptoms in conditions like stroke and Alzheimer's disease— a protein called NOS1AP.

Neurodegenerative diseases can result when brain cells become so hyperactive over time that toxic substances build up, causing the cells to self-destruct.

Though scientists may eventually develop drugs that reverse the process that leads from excitotoxicity to neuron death, the mechanism is still incompletely defined. Researchers knew that over-stimulated neurons produce small quantities of nitric oxide, which is a signal for cell death, but were skeptical that those amounts could be strong enough to lead to brain damage.

A new study, led by researchers at the University of Eastern Finland and published in the Journal of Neuroscience, finds that the NOS1AP protein amplifies the nitric oxide signal and activates a cell destruction initiator molecule called MKK3.

The resulting cascade of cell events shifts the neuron from over-stimulation mode to full-on cell death, or apoptosis.

The Finnish researchers tested a peptide chemical that interfered with NOS1AP in rat neurons, reducing the cell death signal by keeping the protein from seeking out nitric oxide.

The chemical was successful in limiting cell death in a rat model of a type of stroke called hypoxia-ischemia, and the rat brain cells treated with the chemical in the experiment had less damage than those without it.

With more research, the scientists write that the NOS1AP pathway could lead to a future "generation of neuroprotectants with high specificity." The drugs may be able to target the neurodegeneration pathway to prevent brain disorders like stroke, epilepsy, Alzheimer's disease.

NOS1AP is also implicated in conditions as varied schizophrenia, diabetes, and heart attack, raising the possibility that future drugs that act on the protein could also lead to treatments for those diseases as well.