The neurons which receive these neurotransmitters are called catecholaminergic neurons. These oxidation reactions have products which are harmful to neurons. It is known that catecholaminergic neurons decline in number with age, and it has been theorized that the byproducts of catecholamine oxidation are responsible for this decay. The body has mechanisms to detoxify these compounds, since they are toxic to cells in general, which explains why the neurons are not destroyed from these reactions much earlier in life. The age-correlated decay which occurs is attributed to a gradual erosion of neurons from incidental failures of these detoxifying mechanisms, which increase in frequency with age.
Norepinephrine is a catecholamine, and is used as an example in the pathways.
Also shown are the reactions by which the body converts some of these toxins to harmless agents. Because of this, catecholamine-derived quinones are received by the neurons which normally receive the parent catecholamine compound. This renders the neuron inoperable, because the quinone blocks the neuron from receiving any other compounds. Quinones have great facility for reduction, which enables them to absorb the electrical impulses conducted along neurons, further impairing their function. Dopamine is the most harmful catecholamine which occurs naturally, because its autoxidation-produced quinone is especially toxic.