CONTENT OF BRAIN ALUMINUM IS NOT ELEVATED IN ALZHEIMER-DISEASE

Several studies have reported that the bulk aluminum (Al) concentratio n is increased in the brain in Alzheimer disease (AD), while other stu dies have failed to demonstrate an increase. Most of these investigati ons have had one or more methodological deficiencies, including lack o f adequate neuropathological assessment; failure to age-match the cont rol samples; small sample sizes, lacking statistical power; and geogra phical heterogeneity in the AD and control populations. The present po pulation-based study of 92 clinically and histopathologically diagnose d AD patients and normal elderly nursing home residents was designed t o avoid these potential biases. When a subsample of AD cases with the most severe brain pathology was compared with controls having no or mi nimal pathology, no statistically significant differences were found i n the bulk aluminum concentration measured by graphite furnace atomic absorption spectrometry in frontal cortex (1.8+/-0.7 vs. 1.7+/-0.7 mu g/g dry wt), temporal cortex (1.4 +/-0.3 vs. 1.5+/-0.5 mu g/g dry wt), liver (2.0+/-1.3 vs. 2.0+/-1.2 mu g/g dry wt), or head of femur (2.4/-1.6 vs. 2.2+/-1.0 mu g/g ash wt). Within the whole series of 92 case s, there was no difference in the bulk aluminum concentration of the f rontal cortex between individuals diagnosed as definite, probable, and possible cases of AD using the CERAD (Consortium to Establish a Regis try for Alzheimer's Disease) criteria. The density of senile plaques a nd neurofibrillary tangles in frontal and temporal cortex showed no co rrelation with the bulk aluminum concentration. Logistic regression an alyses, which controlled for age and sex, did not influence outcome fo r any of the comparisons, The data show conclusively that in AD, bulk aluminum concentration is not increased in two cortical brain regions that are selectively vulnerable to the neuropathological changes assoc iated with this disorder.