For each neurochemical there is an optimal amount which differs for every individual. Above or below this amount, mental function will not improve markedly or will even decrease. Drug effects may be subtle at first, requiring a period of learning for full realization of its benefits.
The schematic diagram here shows how neurotransmitters carry messages between neurons in the brain. An incoming electric impulse stimulates the transmitter neuron to release the message-carrying neurotransmitter chemical from the packets (vesicles) in which it is stored. The neurotransmitter molecules are released into the gap (synapse) between the nerve endings and then bind to the receptors on the nearby receiver neuron. This second neuron is then stimulated by the neurotransmitter in its receptors to fire an electric impulse, which begins the process over again. In other cases, the receiver neuron releases a hormone signal instead of sending out another electric signal. The left-over neurotransmitter in
the synapse is either destroyed by an enzyme or recycled back into the transmitter vesicles. Because of recent advances in our understanding of these events, it is now possible to modify some aging changes in the brain’s neurochemistry.
Although much remains to be learned in the neurochemistry of memory, a modest amount is understood about how
memories are stored and retrieved in the brain. Specific
chemicals that are involved have been isolated, and their loss
in aging may be compensated for by replacing them with supplemental drugs and nutrients. RNA synthesis is required for memory, and RNA may be a memory-storage molecule; the brain may encode RNA molecules with memory “messages.” As people age, they produce less RNA and, consequently, have less RNA available for use in storing memories. In addition to its memory-storage ability, RNA is also an antioxidant that experiments have shown is capable of increasing the life span of rats by about 20 percent. RNA is one nonprescription chemical available in health food stores that we can use to help keep our minds functioning at a level younger than our years.
CAUTION: RNA, however, should not be used by individuals with gout. If gout runs in your family, it is very important to have your doctor test you before taking RNA. When nucleic acids are metabolized, uric acid is formed which, in excessive concentration, can precipitate in joints and kidneys,leading to disability and severe pain. Permanent damage can
be done to the joints and kidneys by these crystals. Moreover, the oxidation of RNA to uric acid by the enzyme xanthine oxidase also releases hydrogen peroxide and free radicals. Before using RNA, have an inexpensive clinical laboratory blood test for uric acid. If your serum uric acid and kidneys are normal, you should be able to use oral RNA. (Severe allergic reactions sometimes occur with RNA injections.)
Even if RNA is contraindicated for you, you can take vitamin B-12, which stimulates RNA synthesis in brain neurons. Its administration in rats increased their rate of learning. A dose of 1,000 micrograms (1 milligram) is a reasonable daily dose for an adult human. We know of no evidence that B-12 poses a hazard to people with gout, but suggest that such people watch their urate level while using B-12 to see that it doesn’t rise.
Another chemical system involved in memory consolidation (transfer of short-term memories into long-term storage) is the cholinergic system. Acetylcholine is a neurotransmitter in the brain which is thought to be centrally involved in memory. Experiments in humans in which the anticholinergic drug scopolamine was administered to healthy young per-
sons resulted in a pattern of memory deficit that was very like that of senile old age. The nutrients choline and lecithin (which contains phosphatidyl choline) and the drug Deaner® can supply the brain with the choline it needs to manufacture acetylcholine. Plenty of vitamin B-5 (calcium pantothenate or pantothenic acid) is required for this conversion.
In a very recent mouse study, 13-month-old mice on a choline-enriched diet performed as well as 3-month-old mice on a learning retention task, whereas 13-month-old mice on a choline-deficient diet performed as poorly as senescent (23 months and older) mice. A choline-deficient diet in younger animals may result in learning retention more typical of that of older animals because the older animals cannot produce as much acetylcholine in their brains. Choline has been experimentally demonstrated in humans to improve memory and serial-type learning (a series of words, for example). A single oral dose of 10 grams of choline produced these results. In a study mentioned earlier involving MIT students, 3 grams per day was effective in improving memory and serial learning. The old wives’ tale that fish is brain food really has a degree of truth, since fish contains relatively large quantities of both choline and RNA
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