Page 172 - The Memory Program How to Prevent Memory Loss and Enhance Memory Power
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                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.


            Different Ways to Boost Acetylcholine

            Cholinesterase inhibitors are compounds that inhibit the action of this enzyme, acetylcholinesterase.
            Treatment with cholinesterase inhibitors indirectly raises the level of acetylcholine by preventing its
            breakdown, thereby leading to improved attention, mental arousal, learning, and memory. In fact,
            cholinesterase inhibitors have now reached the forefront of treatment in Alzheimer's disease, and
            memory loss more broadly.

              If you step back for a moment and think about the issue, this indirect approach does seem a bit
            odd. Why not directly increase the amount of acetylcholine by pouring it directly into the synapse, or
            administer a substance (precursor) that is converted to acetylcholine in the brain? Well, these
            strategies have been tried with compounds like choline and lecithin.
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