When Quinolinic acid increases to pathological levels it becomes an exitotoxin that over-activates NMDA receptors. This causes a rapid inflow of calcium into the neuron and the resulting chaos leads to mitochondrial dysfunction, ATP exhaustion, free radical formation, oxidative damage, and cell death signaling.
Mice bred to develop Alzheimer's-like symptoms were given a drug that increased sensitivity to hormones shown to combat diabetes. The mice showed memory improvement to near normal levels.
An FDA approved drug reduces energy requirements in neurons. Relieved from the pressure of protein production the mitochondria can produce energy for cellular repair processes.