many common brain problems are not caused by deficits of
neurotransmitters, but rather by neurotransmitters that are
unable to work the way they ought to, due to an induced or
underlying dysfunction. Similarly, dementia is not caused
by low acetylcholine, a neurotransmitter involved in
memory; acetylcholine is low because the neurons that
produce it are, in many cases, slowly dying.
This is why such drugs have no “disease-modifying”
ability—meaning, they do nothing to solve the underlying
problems that create the package of symptoms that we see
as “dementia.” They act merely as Band-Aids. Attention
deficits, memory loss, and depressed mood may all be
manifestations of underlying problems, and pharmaceuticals
continually come up short.
HOW NEUROTRANSMITTERS WORK
For a microscopic system, neurotransmitter function is an
incredibly elegant design. Some of the neurotransmitter gets
released by a neuron. This neuron is called the presynaptic
cell because it initiates the message and thus comes before
the synapse. The neurotransmitter then moves into the
synaptic cleft, which is the gap between neurons. There,
molecules of neurotransmitter cross the gap to meet a
receptor on the receiving, or postsynaptic, neuron. The
leftover neurotransmitter is either taken back up by the
presynaptic cell, called reuptake, or degraded by enzymes.
Under normal conditions, this postsynaptic “cleanup” is
done to prevent excessive stimulation of the postsynaptic