Recent evidence indicates that those at risk of developing
Parkinson’s disease have a defect in iron metabolism.26
In this study, Parkinson patients’ total iron binding capacity
and transferritin saturation were significantly lower than
that of controls, with no difference in their dietary intake of
iron. Other researchers have found increased iron and aluminum
in the neuromelanin pigment in the substantia nigra
of Parkinson’s patients.27 Aluminum appears to displace
iron from the ferritin molecule, thereby increasing the interaction
of iron during the hydrogen peroxide interaction with
superoxide. This reaction forms the powerful hydroxyl radical.
28
In the brains of Alzheimer’s disease patients, aluminum,
iron, and mercury are consistently found in elevated
concentrations in affected neurons,29 transferritin levels
are decreased, and iron, ferritin, and transferritin are concentrated
around the senile plaques.
ALUMINUM AND NEURODEGENERATION
The connection between aluminum exposure and brain
dysfunction was strengthened when several dialysis units
reported patients with an unusual dementing syndrome related
to elevated aluminum levels in the dialyslate.30 Once the
dialysis water was cleared of aluminum, the dementing syndrome
disappeared. Based on this finding, others began to suspect
aluminum toxicity as an etiology of Alzheimer’s disease.
One early study, in which individuals were examined in
88 counties in England and Wales, areas with elevated aluminum
levels in the drinking water had higher incidences of
Alzheimer’s dementia.31 A later, more well-controlled
study found that elderly people who drank water high in
aluminum had a 4.4X higher incidence of Alzheimer’s disease
than those who drank water with lower levels.32
After this suggestive research, more accurate studies
were conducted for measuring brain levels of aluminum in
several neurodegenerative disorders. Despite early conflicting
results, the latest studies performed with microtechnique
high-tech laser and x-ray probes clearly indicate elevated
levels of aluminum in the area of neurofibrillary tangles
in Alzheimer’s disease.33 Similar results have been
found in cases of Parkinson’s disease.34 The results of one
ALS study indicated that while spinal cord levels of aluminum
were not elevated above controls, they did find a
1.5- to 2-fold elevation in iron and calcium.35 Using more
sophisticated methods, another study confirmed the earlier
finding of elevated aluminum levels in the motor neurons of
ALS patients.36
Besides increasing free radical generation, aluminum
has several other negative effects on cell function. One
study found that primates exposed to excess aluminum had
a significant decrease in total lipid, glycolipid, and phospholipid
content in their brains.37 Aluminum also damages
membrane-bound enzymes such as Na+-K+ATPase, acetylcholinesterase,
and 2’, 3’-cyclic nucleotide phosphohydrolase,
all enzymes necessary for normal neuron function.
A recent study found that aluminum in the presence of
melanin significantly enhanced lipid peroxidation.38 This is
important in the case of Parkinson’s disease, since the neuromelanin-
containing cells of the substantia nigra are the
cells most affected by the disease. Of enormous importance
is the finding that high aluminum levels can inhibit the
activity of many antioxidant enzymes, such as catalase,
superoxide dismutase, and glutathione peroxidase.39
Several studies have linked aluminum to formation of
the paired helical filaments found in Alzheimer’s disease.40
Aluminum appears to interfere with dephosphorylation of
the hyperphosphorylated tau protein. Experimentally, using
the aluminum-chelating agent desferrioxamine, researchers
could reverse this resistance to aluminum-induced dephosphorylation.
41
The entry of aluminum into the brain, past the bloodbrain
barrier, is significantly enhanced when aluminum is
bound to glutamate.42 Once in the brain, aluminum has
been shown to potentate excitotoxicity by enhancing glutamate-
triggered calcium accumulation within the neuron,43
and to increase the formation of iron-induced free radicals.
Is aluminum the only cause of these neurodegenerative
diseases? I don’t think so. However, I do think that it is a significant
contributing factor. Numerous environmental agents,
viruses, autoimmune disorders, and injuries can all trigger the
same central destructive mechanism—excitotoxicity. Often
we see several of these factors coexisting in the same person.
At high risk is the person having mineral deficiencies, poor
nutritional supply of antioxidants, and antioxidant enzyme
deficiencies.
It is interesting to note that gastrointestinal absorption
of aluminum was found to be enhanced in Down’s syndrome,
a condition with pathological features similar to
Alzheimer’s disease.44 In this study, aluminum absorption
in Down’s syndrome was 4X greater when absorbed as an
antacid, and 6X higher in the presence of citrate than that
seen in controls. Another study found that adding citrate to
aluminum hydroxide antacid increased absorption as much
as 11X in normal adults.45 This may be a good reason to not
add lemon juice to your tea, since tea is high in aluminum
and lemons are high in citrate.
A monocarboxylic acid transporter controls entry of
aluminum into the brain. Pyruvate competes with aluminum
citrate for entry, thereby providing a way to inhibit
brain accumulation of aluminum.46 Pyruvate, as well as
malate, have also been shown to inhibit glutamate toxicity.47
INFLAMMATION, CYTOKINES AND
AUTOIMMUNITY
For many years scientists suspected that the immune