This summary attempts to clarify associations,which
have drawn considerable attention, between smoking,
nicotine, nicotinic receptors, and AD. Some general
principles and critical questions emerge that might
guide continuing work to elucidate these relationships.
One principle is that tobacco smoking is certainly not
equivalent to direct administration of nicotine. Tobacco
contains thousands of compounds, many of which are
known to be toxic, that could negate any neuroprotective
or acute cognition-enhancing effects of nicotine.
Thus, it would be surprising if smoking behavior affected
the incidence or progression of symptoms of AD
in the same way as nicotine or nicotinic drugs. Nevertheless,
an important lead would be indicated if smoking
behavior indeed is shown to produce lower incidence
of AD. Another is that smoking behavior and
nicotinic drugs may have beneficial effects on only a
subset of the population, just as smoking behavior itself
is a feature of only a subset of individuals. More work
is needed to determine more precisely the therapeutic
objectives in potential nicotinic drug treatment of dementia
and to establish the mechanism(s) involved in
any cognition-enhancing effects of such treatment or of
smoking behavior.