Increase in acetylcholine leads to improved attention, mental arousal, and memory.
From age forty to ninety, the nucleus basalis of Meynert gradually and progressively loses up to half its cholinergic nerve cells.
This loss of cholinergic nerve cells causes a delay in the brain's ability to process information quickly and accurately, which is why aging leads to slower reactions as well as to mild memory loss.
In Alzheimer's disease, the nucleus basalis is nearly wiped out within a few years after clinical onset of the illness, causing severe memory loss.
Cholinergic nerve cells release acetylcholine into a narrow cleft or space called the synapse. This acetylcholine molecule races across the synapse and latches onto a receptor in the next neuron, called the postsynaptic neuron. The postsynaptic receptor is specially configured for the acetylcholine molecule, the way a keyhole receives a key. Attachment to this receptor triggers a series of biochemical and physiologic events in the postsynaptic or receiving neuron, leading to a change in brain function that involves improved mental arousal and memory. Once acetylcholine completes its job, it is either sucked back by the nerve cell that released it, ready to fight another day, or it is broken down by the enzyme acetylcholinesterase in the synaptic cleft.
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