Some smart drugs can be found in health food stores;
others are imported or are drugs that are intended for other disorders
like Alzheimer's disease and Parkinson's disease. There are many Internet
web sites, books, magazines and newspaper articles detailing the supposed
effects of smart drugs. There are also plenty of advertisements and
mail-order businesses that try to sell "smart drugs" to the
public. However, rarely do these businesses or the popular press report
results that show the failure of smart drugs to improve memory or learning.
Rather, they try to show that their products have miraculous effects
on the brain and can improve mental functioning. Wouldn't it be easy
to learn something by "popping a pill" or drinking a soda
laced with a smart drug? This would be much easier than taking the time
to study. Feeling dull? Take your brain in for a mental tune up by popping
a pill!
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Some data suggest that cognitive enhancers do improve
some types of learning and memory, but many other data say these substances
have no effect. The strongest evidence for these substances is for the
improvement of cognitive function in people with brain injury or disease
(for example, Alzheimer's disease and traumatic brain injury). Although
"popular" books and companies that sell smart drugs will try
to convince you that these drugs work, the evidence for any significant
effects of these substances in normal people is weak. There are also
important side-effects that must be considered. Many of these substances
effect neurotransmitters systems in the central nervous system. The
effects of these chemicals on neurological function and behavior is
unknown. Moreover, the long-term safety of these substances has not
been adequately tested. Also, the possibility that these substances
will interact with other substances a person might take is untested.
A substance like the herb Ma-huang may be dangerous if a person stops
taking it suddenly.
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Many
of the positive effects of cognitive enhancers have been seen in experiments
using rats. Scientists train rats on a specific test, like running in
a maze, and then see if the "smart drug" can improve the rats'
performance. It is difficult to see how many of these data can be applied
to human learning and memory. For example, what if the "smart drug"
made the rat hungry? Wouldn't a hungry rat run faster in the maze to
receive a food reward than a non-hungry rat? Maybe the rat did not get
any "smarter" and did not have any improved memory. Perhaps
the rat ran faster simply because it was hungrier. Therefore, it was
the rat's motivation to run the maze, not its increased cognitive ability
that affected the performance. Thus, it is important to be very careful
when interpreting changes observed in these types of animal learning
and memory experiments.
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One
symptom of Alzheimer's disease is a reduced brain level of the neurotransmitter
called acetylcholine. It is thought that an effective treatment for
Alzheimer's disease might be to increase brain levels of acetylcholine.
Another possible treatment would be to slow the death of neurons that
contain acetylcholine. Two drugs, Tacrine and Donepezil, are both inhibitors
of the enzyme (acetylcholinesterase) that breaks down acetylcholine.
These drugs are approved in the US for treatment of Alzheimer's disease.
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