Felice wrote:
>
> OT PS for denture users: My neurologist and hematologist think my ataxia may
> have resulted from a copper deficiency after years of using denture adhesive
> with high zinc content, even though I stopped using it when I went the
> implant route. Those of you who have been using it for a while may want to
> check www.neurology.com using keywords "copper dentures", and consider
> asking your PCPs about having your copper levels checked. Disclaimer: This
> is not medical advice!

On the other hand, be cautious about going overboard
in the other direction.


J Alzheimers Dis. 2007 Jun;11(3):371-83.
A rabbit model of Alzheimer's disease: valid at
neuropathological, cognitive, and therapeutic
levels.
Woodruff-Pak DS, Agelan A, Del Valle L.
Department of Psychology, Temple University,
Philadelphia, PA 19122, USA.

Supplementing a rabbit's diet with 2% cholesterol
alone or with a trace amount of copper created
neuropathological changes that resembled those seen
in Alzheimer's disease (AD). AD model rabbits were
impaired in eyeblink classical conditioning; a form
of learning severely impaired in AD. Our aim was
to replicate AD rabbit model neuropathology, test
eyeblink conditioning in this model, and determine
if galantamine (Razadyne) would ameliorate impaired
conditioning. In Experiment 1 rabbit chow with 2%
cholesterol and drinking water with 0.12 mg/liter
copper sulfate were administered for 10 weeks.
Control rabbits received normal food and water.
Rabbit brains were probed for neuropathology. AD
model rabbits had significant neuronal loss in
frontal cortex, hippocampus and cerebellum. Changes
in neurons in the hippocampus were consistent with
neurofibrillary degeneration and cytoplasmic
immunoreactivity for amyloid-beta and tau.
In Experiment 2 AD model rabbits were injected
daily with vehicle or 3.0 mg/kg galantamine and
tested on 750 ms trace and delay eyeblink
conditioning. Galantamine improved eyeblink
conditioning significantly over vehicle. The AD
rabbit model has validity from neuropathological
to cognitive levels and offers a promising
addition to the available animal models of AD.
Galantamine ameliorated impaired eyeblink
conditioning, extending the validity of the AD
rabbit model to treatment modalities.


Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11065-9.
Trace amounts of copper in water induce beta-amyloid
plaques and learning deficits in a rabbit model
of Alzheimer's disease.
Sparks DL, Schreurs BG.
Sun Health Research Institute, 10515 West Santa Fe
Drive, Sun City, AZ 85351, USA.

Despite the crucial role played by cholesterol and
copper in nutrition and normal brain function,
recent evidence indicates that they may both be
important factors in the etiology of Alzheimer's
disease (AD). Here we provide critical evidence
for the role of cholesterol and copper in AD by
showing that the addition of trace amounts of
copper (0.12 ppm) to water given to cholesterol-fed
rabbits can induce beta-amyloid (Abeta)
accumulation, including senile plaque-like
structures in the hippocampus and temporal lobe,
and can significantly retard the ability of rabbits
to learn a difficult trace conditioning task. The
Abeta deposits do not affect the ability of rabbits
to detect or respond to the training stimuli nor to
learn a simpler delay conditioning task. Trace
amounts of copper in drinking water may influence
clearance of Abeta from the brain at the level of
the interface between the blood and
cerebrovasculature and combined with high
cholesterol may be a key component to the
accumulation of Abeta in the brain, having a
significant impact on learning and memory.
Cholesterol-fed rabbits have at least 12
pathological markers seen in AD, suggesting that
the cholesterol-fed rabbit is a good animal model
for studying AD.