Bone aluminium content in Alzheimer's disease
D O'Mahony1, J Denton, J Templar
1Mercer's Institute for Research on Ageing, St. James's Hospital, Dublin, Ireland.
Dementia (Basel, Switzerland)
|March 1, 1995
Summary
This study found lower bone aluminium levels in Alzheimer's patients, suggesting excessive aluminium absorption is unlikely to cause the disease. Further research is needed to understand aluminium's role in Alzheimer's disease.
Area of Science:
- Neuroscience
- Toxicology
- Gerontology
Background:
- The link between aluminium exposure and Alzheimer's disease (AD) remains debated.
- Aluminium neurotoxicity is a potential factor in AD pathophysiology, possibly due to excessive exposure or impaired brain uptake.
- Investigating long-term aluminium exposure is crucial for understanding its role in AD.
Purpose of the Study:
- To evaluate trabecular bone aluminium content as a marker of long-term aluminium exposure in patients with senile dementia of the Alzheimer type (SDAT).
- To test the hypothesis that excessive aluminium absorption and accumulation contribute to Alzheimer's disease.
- To compare bone aluminium levels in SDAT patients with age-matched controls.
Main Methods:
- Trabecular bone samples were obtained from femoral neck fracture specimens during hip replacement surgery.
- Quantitative analysis of bone aluminium content was performed using atomic absorption spectrometry.
- Qualitative histological analysis utilized the acid solochrome azurine staining technique.
Main Results:
- Quantitative analysis revealed significantly lower bone aluminium content in SDAT patients (11.9 µg/g) compared to controls (18.2 µg/g) at the 95% confidence limit.
- Qualitative histological examination did not detect significant aluminium deposition in bone samples from either group.
- These findings do not support the hypothesis of excessive aluminium absorption in Alzheimer's disease.
Conclusions:
- The study's results do not support the hypothesis that excessive aluminium absorption and subsequent tissue accumulation are implicated in the pathophysiology of Alzheimer's disease.
- Lower bone aluminium levels in SDAT patients suggest impaired aluminium absorption or altered distribution rather than excessive accumulation.
- Further investigation into the mechanisms of aluminium uptake and its specific role in neurodegeneration is warranted.
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