Last I'd heard, the aluminum/Alzheimer link was on the
outs. But key words " alzheimer aluminum " at PubMed
(http://www.ncbi.nlm.nih.gov/PubMed) found several
resent studies suggesting a connection. In fact,
one study, the abstract of which is below, states:
"Excess, insoluble amyloid beta protein (A beta)
contributes to AD [Alzheimer's disease]. Aluminum
promotes formation and accumulation of insoluble
A beta and hyperphosphorylated tau."
Neurotoxicology, 2000 Oct;21(5):813-28.
This suggests to me that researchers have found that
aluminum Can play a contributory role in AD pathology.
Conclusion: "These findings support the hypothesis that
a high concentration of aluminum in drinking water may
be a risk factor for Alzheimer's disease."
Am J Epidemiol 2000 Jul 1;152(1):59-66
Relation between aluminum concentrations in drinking water
and Alzheimer's disease: an 8-year follow-up study.
Rondeau V, Commenges D, Jacqmin-Gadda H, Dartigues JF
INSERM Unite 330, Universite Victor Segalen Bordeaux II, France.
To investigate the effect of aluminum and silica in drinking
water on the risk of dementia and Alzheimer's disease, the
authors analyzed data from a large prospective cohort (Paquid),
including 3,777 subjects aged 65 years and over living at home
in 75 civil parishes in Gironde and Dordogne in southwestern
France in 1988-1989. The subjects were followed for up for 8
years with an active search for incident cases of dementia or
Alzheimer's disease. Mean exposure to aluminum and silica in
drinking water was estimated in each area. The sample studied
included 2,698 nondemented subjects at baseline, for whom
components of drinking water and covariates were available. A
total of 253 incident cases of dementia (with 17 exposed to
high levels of aluminum), including 182 Alzheimer's disease
(with 13 exposed to high aluminum levels), were identified.
The relative risk of dementia adjusted for age, gender,
educational level, place of residence, and wine consumption
was 1.99 (95 percent CI: 1.20, 3.28) for subjects exposed to
an aluminum concentration greater than 0.1 mg/liter. This
result was confirmed for Alzheimer's disease (adjusted relative
risk = 2.14, 95 percent CI: 1.21, 3.80). However, no dose-
response relation was found. Inversely, the adjusted relative
risk of dementia for subjects exposed to silica (> or = 11.25
mg/liter) was 0.74 (95 percent CI: 0.58, 0.96). These findings
support the hypothesis that a high concentration of aluminum in
drinking water may be a risk factor for Alzheimer's disease.
Neurotoxicology 2000 Oct;21(5):813-28
The toxicology of aluminum in the brain: a review.
College of Pharmacy and Graduate Center for Toxicology, University
of Kentucky Medical Center, Lexington, USA. firstname.lastname@example.org
Aluminum is environmentally ubiquitous, providing human exposure.
Usual human exposure is primarily dietary. The potential for
significant Al absorption from the nasal cavity and direct
distribution into the brain should be further investigated.
Decreased renal function increases human risk of Al-induced
accumulation and toxicity. Brain Al entry from blood may involve
transferrin-receptor mediated endocytosis and a more rapid process
transporting small molecular weight Al species. There appears to
be Al efflux from the brain, probably as Al citrate. There is
prolonged retention of a fraction of Al that enters the brain,
suggesting the potential for accumulation with repeated exposure.
Al is a neurotoxicant in animals and humans. It has been implicated
in the etiology of sporadic Alzheimer's disease (AD) and other
neurodegenerative disorders, although this is highly controversial.
This controversy has not been resolved by epidemiological studies,
as only some found a small association between increased incidence
of dementia and drinking water Al concentration. Studies of brain Al
in AD have not produced consistent findings and have not resolved
the controversy. Injections of Al to animals produce behavioral,
neuropathological and neurochemical changes that partially model AD.
Aluminum has the ability to produce neurotoxicity by many mechanisms.
Excess, insoluble amyloid beta protein (A beta) contributes to AD.
Aluminum promotes formation and accumulation of insoluble A beta
and hyperphosphorylated tau. To some extent, Al mimics the deficit
of cortical cholinergic neurotransmission seen in AD. Al increases
Fe-induced oxidative injury. The toxicity of Al to plants, aquatic
life and humans may share common mechanisms, including disruption
of the inositol phosphate system and Ca regulation. Facilitation
of Fe-induced oxidative injury and disruption of basic cell processes
may mediate primary molecular mechanisms of Al-induced neurotoxicity.
Avoidance of Al exposure, when practical, seems prudent.
Environ Res 2000 Nov;84(3):234-46
Aluminum forms in drinking water and risk of Alzheimer's disease
Gauthier E, Fortier I, Courchesne F, Pepin P, Mortimer J, Gauvreau D
Departement de Geographie, Universite de Montreal, Montreal, Quebec, Canada.
The objective of this study was to assess the relation between
long-term exposure to different aluminum (Al) forms in drinking
water and Alzheimer's disease (AD). The study participants were
selected from a random sample of the elderly population (>/=70
years of age) of the Saguenay-Lac-Saint-Jean region (Quebec).
Sixty-eight cases of Alzheimer's disease diagnosed according to
recognized criteria were paired for age (+/-2 years) and sex with
nondemented controls. Aluminum speciation was assessed using
established standard analytical protocols along with quality
control procedures. Exposure to Al forms (total Al, total
dissolved Al, monomeric organic Al, monomeric inorganic Al,
polymeric Al, Al(3+), AlOH, AlF, AlH(3)SiO(2+)(4), AlSO(4)) in
drinking water was estimated by juxtaposing the subject's
residential history with the physicochemical data of the
municipalities. The markers of long-term exposures (1945 to onset)
to Al forms in drinking water were not significantly associated
with AD. On the other hand, after adjustment for education level,
presence of family cases, and ApoE varepsilon4 allele, exposure
to organic monomeric aluminum estimated at the onset of the
disease was associated with AD (odds ratio 2.67; 95% CI 1.04-6.90).
On average, the exposure estimated at the onset had been stable
for 44 years. Our results confirm prime the importance of
estimation of Al speciation and consideration of genetic
characteristics in the assessment of the association between
aluminum exposure and Alzheimer's disease. Copyright 2000
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