Many of these conditions are curable. The neurons in the cerebral cortex are the focal site of cellular degeneration in Alzheimer's, but lower brain nuclei that send modulating neurotransmitters to the cortex are also severely affected. The most striking symptoms are produced by acetylcholine depletion-which contributes significantly to loss of memory and loss of capacity for attentiveness. Likewise, attempts to treat patients with drugs that stimulate acetylcholine receptors have been a failure. But acetylcholinesterase inhibitors have proven to be of therapeutic value.
Neurons send signals to other neurons by releasing chemicals into synapses.
But signals are only effective when they have a beginning and an end. You can't send Morse code by applying constant pressure on a telegraph key. Acetylcholinesterase, the enzyme that breaks down acetylcholine, ends the chemical signal that begins when acetylcholine is released into a synapse and then connects with a receptor. The memory loss effect that acetylcholinesterase plays in Alzheimer's may be due to amplification of signals which would have been weakened by neurodegeneration. Huperzine-A has been used for centuries in China as an herbal medicine prepared from the moss Huperzia serrata.