These are some replies from another newsgroup regarding nicotine as a
preventive of Alzheimers..... NOT from smoking, but from gum only.
*****************

Take a look at this, Evelyn.

Effects of nicotinic stimulation on cognitive performance.

Newhouse PA, Potter A, Singh A.

Clinical Neuroscience Research Unit, Department of Psychiatry, University of
Vermont College of Medicine, 1 South Prospect St, Burlington, VT 05403, USA.
Paul.Newhouse@uvm.edu

Recent advances in studies of nicotinic agents in humans have begun to more
carefully define cognitive operations that can be influenced by nicotinic
stimulation and/or blockade. Careful separation of the cognitive domains
affected by nicotinic stimulation has identified attentional performance as
the most likely candidate to be positively influenced by nicotinic receptor
activation. Studies of the effects of nicotinic systems and/or nicotinic
receptor stimulation in pathological disease states such as Alzheimer's
disease, Parkinson's disease, attention deficit/hyperactivity disorder and
schizophrenia show the potential for therapeutic utility of nicotinic drugs.
In contrast to studies in pathological states, studies of nicotine in
normal-non-smokers tend to show deleterious effects. This contradiction can
be resolved by consideration of cognitive and biological baseline dependency
differences between study populations in terms of the relationship of
optimal cognitive performance to nicotinic receptor activity. Although
normal individuals are unlikely to show cognitive benefits after nicotinic
stimulation except under extreme task conditions, individuals with a variety
of disease states can benefit from nicotinic drugs. Attentional
function/dysfunction may serve as an endophenotypic therapeutic target for
nicotinic drug development.

PMID: 15018837 [PubMed]

**************

I never said smoking was protective against AD.
I said nicotine was. Take a look at this. You can
get the full article from PubMed by the PMID
number.

Nicotine attenuates beta-amyloid peptide-induced neurotoxicity, free radical
and calcium accumulation in hippocampal neuronal cultures.

Liu Q, Zhao B.

Laboratory of Visual Processing Information, Center of Brain & Cognitive
Science, Institute of Biophysics, Academia Sinica, Beijing 100101, People's
Republic of China.

1. Recent studies indicate that neuronal loss in Alzheimer's disease (AD) is
accompanied by the deposition of beta-amyloid protein (A beta) in senile
plaques. Nicotine as a major component of cigarette smoke has been suggested
to have a protective effect for neurons against A beta neurotoxicity. 2. Our
present study demonstrates that nicotine protected cultured hippocampal
neurons against the A beta-induced apoptosis. Nicotine effectively inhibits
apoptosis in hippocampal cultures caused by A beta(25-35) or A beta(1-40)
treatment and increase of caspase activity induced by A beta(25-35) or A
beta(1-40). 3. Measurements of cellular oxidation and intracellular free
Ca(2+) showed that nicotine suppressed A beta-induced accumulation of free
radical and increase of intracellular free Ca(2+). 4. Cholinergic antagonist
mecamylamine inhibited nicotine-induced protection against A beta-induced
caspase-3 activation and ROS accumulation. 5. The data show that the
protection of nicotine is partly via nicotinic receptors. Our results
suggest that nicotine may be beneficial in retarding the neurodegenerative
diseases such as AD.

PMID: 14757701 [PubMed]

************

Nicotine (NOT SMOKING) may also be beneficial
in neuropsychiatric diseases.

George

Nicotine and nicotinic receptor involvement in neuropsychiatric disorders.

Newhouse P, Singh A, Potter A.

Clinical Neuroscience Research Unit, Department of Psychiatry, University of
Vermont College of Medicine, 1 South Prospect St., Burlington, VT 05401,
USA. Paul.Newhouse@uvm.edu

Advances in the understanding of the neurobiology of the nicotinic receptor
have started to be matched by an appreciation of the potential role of these
receptors in a variety of neuropsychiatric disorders. While alterations in
nicotinic receptor number and/or function have been associated with such
conditions as Alzheimer's disease for several years, there is increasing
evidence that nicotinic receptor function may play a significant role in
other disorders as well including schizophrenia, Parkinson's disease,
anxiety disorders, and attention deficit-hyperactivity disorder (ADHD).
Research in our laboratory and those of other investigators have utilized
sophisticated psychopharmacological, cognitive, electrophysiological,
neuroimaging and other techniques to assess the impact of nicotinic receptor
modulation on the clinical expression of these disorders. This manuscript
reviews data, both experimental and clinical, relating to the role of
nicotine and/or nicotinic receptor function in a variety of neuropsychiatric
disorders with the perspective of developing appropriate targets for
therapeutic drug development.

Publication Types:
 a.. Review
 b.. Review, Academic

PMID: 14754447 [PubMed]